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Immunology > Immunology 2 > Flashcards

Immunology 2 Flashcards

1
Q

What kind of cell is a T cell and where is it produced?

A

T cells are lymphocytes (derived from common lymphoid precursor) that are produced in the bone marrow

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2
Q

T cells for the most part migrate and mature in _________ and differentiate into cells with what function?

A

Migrate and mature in the thymus, and differentiate into cells that either kill target cells that bear their cognate peptide:MHC class I complex or supply help to other immune cells by cytokine production.

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3
Q

T or F: T cells only recognize peptide antigen.

A

T

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4
Q

T or F: T cells secrete immunoglobulin molecules.

A

F

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5
Q

What is the structure of T cell receptors (TCR)?

A

They’re disulfide-linked heterodimers that consist of either an alpha and beta chain or a gamma and delta chain.

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6
Q

What TCR do most T cells have?

A

Alpha/beta

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7
Q

The variable domain is located near the ________ end of a TCR chain, and the constant domain is located near the _________ end.

A

Amino-terminal: variable domain

Carboxyterminal: constant domain

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8
Q

What is located at the extreme end of the carboxyterminal region of each chain in a TCR? What function does this serve?

A

A hinge-like region, followed by a transmembrane region and a short cytoplasmic tail. This region of the TCR anchors it into the T cell membrane and allows molecule flexibility

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9
Q

What does the TCR resemble structurally and functionally?

A

A membrane-bound antibody Fab fragment

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10
Q

T or F: Somatic recombination is used to construct the variable regions of the TCR complex.

A

T

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11
Q

Gamma/delta T cells are found primarily where?

A

Mucosal epithelium

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12
Q

T or F: Both alpha/beta and gamma/delta T cells are restricted to peptide antigens presented in context with MHC proteins.

A

F: Alpha/beta T cells are restricted, but gamma/delta T cells are not MHC restricted in their recognition of antigen

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13
Q

Gamma/delta T cells primarily recognize _______.

A

Non-protein antigenic determinants (lipid antigens, carb antigens)

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14
Q

T or F: Gamma/delta T cells mature extrathymically.

A

T

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15
Q

T or F: Mature alpha/beta T cells can express CD4, CD8, or both.

A

F: Can express either but not both

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16
Q

What is the signal transduction unit for the T cell receptor?

A

CD3

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17
Q

How do ITAMs (immunoreceptor tyrosine-based activation motifs) initiate a signaling cascade?

A

ITAMs associate with protein tyrosine kinases, which phosphorylate Tyr residues in the ITAMs. Enzymes then bind to the phosphorylated Tyr residues and become activated. This initiates a signaling cascade.

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18
Q

CD4 binds weakly to ____ on the surface of antigen-presenting cells.

A

MHC class II molecules

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19
Q

What’s the function of CD4+ T cells?

A
  • Produce cytokines and provide help to B cells

- Upregulate the cells of the innate immune system

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20
Q

What is the basic structure of CD4?

A

Single chain protein with an extended structure

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21
Q

What is the basic structure of CD8?

A

Hereodimer formed by an alpha and beta chain connected by a disulfide bond

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22
Q

CD8 binds weakly to _______ on the surface of antigen presenting cells or target cells.

A

MHC class I molecules

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23
Q

What is the function of CD8+ T cells?

A

Kill cells that are presenting their cognate peptide antigen via MHC class I

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24
Q

What comprises the CD3 complex?

A

1 CD3 gamma chain, 1 CD3 delta chain, 2 CD3 epsilon chains, and 1 zeta homodimer

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25
Q

Where are ITAMs?

A

On the cytoplasmic tails of CD3 molecules

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26
Q

What functions can accessory molecules perform?

A
  1. Activation of T cell
  2. Tighter interaction of T cell and APC
  3. Killing of a target cell
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27
Q

What is CD45/what does it do?

A

AKA common leukocyte antigen. It’s a protein tyrosine phosphatase accessory molecule that is involved in T cell activation.

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28
Q

What does CD28/CTLA-4 do?

A

Binds to the B7 molecule on antigen processing cells, which delivers a costimulation signal to the T cell (this signal is required for T cell activation!)

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29
Q

What does CD5 do?

A

When it binds its ligand on B cells it promotes activation of T cells

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30
Q

What does Fas ligand (FasL) do?

A

Binds to Fas expressed on the surface of target cells, initiating Fas-mediated apoptosis

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31
Q

What functions do adhesion cells provide?

A

They primarily strengthen the interaction between a T cell and APCs or target cells, but they may also promote activation of T cells

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32
Q

What does lymphocyte function antigen (LFA-1) do?

A

It interacts with intracellular adhesion molecules (ICAM-1, ICAM-2, and ICAM-3) on target cells.

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33
Q

What does CD2 do?

A

Binds to LFA-3 on target cells and promotes cell-to-cell adhesion and T cell activation

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34
Q

What do very late antigens (VLAs) do?

A

They’re expressed on activated cells later in the response, and they bind to fibronectin on target cells to enhance the interaction between the T cell and the target cell

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35
Q

What is the function of lymphokine receptors?

A

They function to activate protein kinase cascades that deliver signals to the nucleus of the T cell

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36
Q

Each thymus lobule is separated into ______ and ______.

A

A cortex and medulla

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37
Q

What cells primarily populate the cortex of the thymus?

A

Thymocytes and cortical epithelial cells (CE cells express MHC class I and II antigens)

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38
Q

T or F: The cortex of the thymus is heavily populated with macrophages and bone marrow derived dendritic cells.

A

F: there are very few of these

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39
Q

What cells populate the medulla of the thymus?

A

Medullary epithelial cells, dendritic cells, and macrophages

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40
Q

T or F: Bone marrow derived macrophages and dendritic cells in the medulla of the thymus express class I and II MHC antigens.

A

T

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41
Q

When is the human thymus fully developed?

A

At birth

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42
Q

When is the rate of T cell production in the thymus the greatest?

A

Before puberty

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43
Q

T or F: Once the T cell repertoire has formed, new T cells are required to sustain T cell mediated immunity.

A

F

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44
Q

Where does massive proliferation of thymocytes occur?

A

In the cortex of the thymus

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45
Q

Where does thymocyte maturation occur?

A

In the medulla of the thymus

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46
Q

Where does positive selection for T cells with TCR that can bind to self-MHC occur?

A

In the cortex of the thymus; non-binders undergo apoptosis

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47
Q

Where does negative selection for T cells with specificity for self occur?

A

In the medulla of the thymus

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48
Q

What are tangible body macrophages?

A

Macrophages that have a unique staining pattern due to the chromatin of phagocytosed thymocytes that underwent apoptosis

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49
Q

What surface markers do thymocytes entering the thymic cortex have?

A

CD4-CD8- (double negative)

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50
Q

When do thymocytes become double positive?

A

Shortly after entering the thymic cortex from the bone marrow

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51
Q

T or F: Double positive thymocytes rapidly divide.

A

True dat.

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52
Q

What do TCRs on developing thymocytes need to continue development?

A

Survival signals or else they’ll die :(

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53
Q

Double positive cells (CD4+CD8+) that survive positive selection differentiate into ______ cells.

A

Single positive T cells (CD4+CD8- or CD4-CD8+)

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54
Q

When does a thymocyte become CD4+CD8-?

A

When the TCR binds to MHC class II

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55
Q

When does a thymocyte become CD4-CD8+?

A

When the TCR binds to MHC class I

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56
Q

Why is the positive selection step in the thymus important?

A

Because the function of mature T cells depends on their ability to bind to either MHC class I or MHC class II molecules. If the TCR has no MHC affinity, no sampling of T cell receptor complexes for cognate peptide antigen will be possible

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57
Q

Where does selection for single positive cells take place?

A

At the cortico-medullary junction of the thymus

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58
Q

What cells are responsible for negative selection of self-reactive T cells?

A

Thymic medullary antigen-presenting cells

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59
Q

What are autoimmune regulators (AIREs)?

A

Transcription factors that cause the expression of several hundred host tissue-specific proteins by epithelial cells in the medulla. When they’re taken up by APCs, they can increase the efficiency of negative selection in the medulla.

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60
Q

Patients that lack functional ________ typically present with autoimmune polyglandular syndrome type I or APECED.

A

AIRE (autoimmune regulator)

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61
Q

How is the alpha chain coding region of the variable region of the TCR produced?

A
  1. VJ junction is formed
  2. Transcription
  3. VJ joins C region
  4. Translation
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62
Q

How is the beta chain coding region of the variable region of the TCR produced?

A
  1. DJ junction is formed
  2. V segment joins DJ to form VDJ junction
  3. Transcription
  4. VDJ joins C region
  5. Translation
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63
Q

Rearrangement of the alpha TCR chain is analogous to _____.

A

Rearrangement of light chain Ig genes

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64
Q

Rearrangement of the beta TCR chain is analogous to ______.

A

Rearrangement of heavy chain Ig genes

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65
Q

In TCR gene rearrangement, which chain genes are the first to rearrange?

A

Beta, gamma, and delta

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66
Q

Thymocytes that bind best to MHC class I molecules will up-regulate (CD4/CD8) expression and down-regulate (CD4/CD8) expression.

A

Upregulate CD8

Downregulate CD4

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67
Q

Thymocytes that bind best to MHC class I molecules will up-regulate (CD4/CD8) expression and down-regulate (CD4/CD8) expression.

A

Upregulate CD4

Downregulate CD8

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68
Q

What is the organization of the TCR alpha chain locus?

A

[LV x 70-80] [J x 61] [C]

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69
Q

What is the organization of the TCR beta chain locus?

A

[LV x 52] [D1] [J1 x 6] [C1] [D2] [J2 x 7] [C2]

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70
Q

T or F: Alpha chain gene rearrangement happens after beta chain gene rearrangement.

A

T

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71
Q

What can surface phenotypes of T cell tumors tell you?

A

When/where a neoplastic event takes place

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72
Q

What is the characteristic cell surface marker of stem cells? Where is it?

A

CD34

Bone Marrow

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73
Q

What are the characteristic cell surface markers of lymphoid progenitor cells? Where are they and what disease is associated with them?

A

CD10, CD19, CD20
Thymus
Common acute lymphoblastic leukemia

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74
Q

What is the characteristic cell surface marker of thymic stromal cells or thymic epithelial cells? Where is it and what disease is associated with it?

A

Cytokeratins
Thymus
Thymoma

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75
Q

What is the characteristic cell surface marker of thymocytes? Where is it and what disease is associated with it?

A

CD1
Thymus
Acute lymphoblastic leukemia

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76
Q

What are the characteristic cell surface markers of T cells? Where are they and what diseases are associated with them?

A 
CD3/TCR, CD4, CD8
Located in the periphery
Sezary syndrome
Adult T cell leukemia
Mycosis fungoides
Chronic lymphocyte leukemia
T prolymphocytic leukemia
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77
Q

What signals are required for activation of naive T cells?

A
  1. TCR recognition of cognate peptide:MHC complex

2. Co-stimulation signal (B7 binding to CD28)

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78
Q

Naive T cells are activated by _______.

A

Professional antigen-presenting cells bearing the T cell’s cognate peptide bound to either MHC class I or MHC class II

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79
Q

What cells express B7 molecules?

A

APCs

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80
Q

How do naive T cells enter the lymphoid organs and what mediates this procesS?

A

By crossing the walls of high epithelial venues (HEV); mediated by adhesion molecules

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81
Q

What is L-selectin and what does it do?

A

It’s an adhesion molecule expressed by naive T cells, and it binds to carbohydrate moieties of vascular addressing that are expressed on the surface of HEVs. This interaction initiates a rolling interaction that results in diapedesis.

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82
Q

How is L-selectin involved in the process of T-cell diapedesis?

A
  1. L-selectin expressed by naive T cells binds to carbohydrate moieties of vascular addressins (CD34 and GlyCAM-1) on the surface of HEVs
  2. Chemokines bound to the surface of HEVs activate LFA-1 (lymphocyte-function-associated-antigen-1)
  3. LFA-1 binds to ICAM-1 (intracellular adhesion molecule-1) on the HEV
  4. The tight interaction allows the T cell to squeeze between two endothelial cells and enter the secondary lymphoid tissue
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83
Q

As they recirculate through the lymphoid tissues, T cells make contact with thousands of antigen-presenting cells every day. What does this allow?

A

It allows sampling of MHC:peptide complexes, so that each T cell has a high probability of encountering antigens derived from pathogens at any site of infection.

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84
Q

T or F: Contact between naive T cells and dendritic cells acts as a survival signal for the T cell.

A

T

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85
Q

If a T cell encounters its cognate peptide:MHC complex, LFA-1 undergoes a conformational change that increases its affinity for ______.

A

ICAMs

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86
Q

What happens to naive T cells that do not encounter specific antigen?

A

They eventually reach the medulla of the lymph node, enter the lymphatic vessel, return to the bloodstream, and recirculate back to other secondary lymphoid tissues

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87
Q

What are the classes of cell-surface adhesion molecules?

A
  1. Selectins
  2. Mucin-like vascular addressing
  3. Integrins
  4. Immunoglobulin superfamily members
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88
Q

What are selectins and what are examples?

A

Lectins that bind to carbohydrates

Ex: L-selectin and P-selectin

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89
Q

What are mucin-like vascular addressins and what are examples?

A

Have carbohydrate moieties that are targets for selection binding
Ex: CD34, GlyCAM-1, MAdCAM-1

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90
Q

What are integrins and what’s an example?

A

They bind to various cell adhesion molecules

Ex: LFA-1

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91
Q

What are immunoglobulin superfamily members targets for? What are examples?

A

Targets for integrin binding

Ex: ICAMs, CD2, LFA-3

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92
Q

What are the types of antigen presenting cells?

A
  1. Dendritic cells
  2. Macrophages
  3. B cells
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93
Q

Which type of APC is most efficient at presentation of viral peptide antigens?

A

Dendritic cells

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94
Q

Which type of APC is best at capturing extracellular organisms such as bacteria and yeast, but can also present antigens derived from intracellular pathogens?

A

Macrophages

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95
Q

Which type of APC is best at presenting peptide from soluble antigens and can present antigens derived from intracellular and extracellular sources?

A

B cells

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96
Q

Where can you find the different types of APCs?

A

Dendritic cells: throughout the body
Macrophages: lymphoid tissue, connective tissue, body cavities
B cells: lymphoid tissue, peripheral blood

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97
Q

What antigens do the different APCs present?

A

Dendritic cell: peptides, viral antigens, allergens
Macrophages: particulate antigens, intra/extracellular pathogens
B cell: soluble antigens, toxins, viruses

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98
Q

What are the most potent antigen-presenting cells?

A

Dendritic cells

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99
Q

T or F: Immature dendritic cells are active in presenting antigen.

A

F: They’re very active in taking up antigen, but they don’t present antigen

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100
Q

Mature dendritic cells are also known as ______.

A

Interdigitating reticular cells

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101
Q

What are Langerhans’ cells?

A

Immature dendritic cells of the skin

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102
Q

What do mature dendritic cells express?

A
  1. Co-stimulatory molecules
  2. High levels of MHC class I and II
  3. Adhesion molecules
  4. DC-CK- a chemokine that attracts naive T cells
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103
Q

T or F: Resting macrophages express low levels of MHC class II and do not express B7.

A

T

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104
Q

What is peripheral tolerance?

A

Macrophages that encounter antigen in absence of bacterial products with present antigen at low levels but won’t supply co-stimulation signals to T cells

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105
Q

Macrophages that ingest microorganisms up-regulate their expression of ____ and ____.

A

MHC and B7 molecules

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106
Q

T or F: B cells constitutively express B7 costimulator molecules.

A

F

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107
Q

What does the signaling through CD28 on the T cell do?

A

Stabilizes IL-2 mRNA and activates the transcriptional activators AP-1 and NF-KB, both of these increase expression of IL-2

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108
Q

What happens to a T cell that recognizes its specific antigen bound to MHC but doesn’t receive the co-stimulation signal?

A

It becomes anergic

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109
Q

Which cells need more co-stimulation: CD4+ or CD8+?

A

CD8+

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110
Q

What does activation by an APC other than a dendritic cell require?

A

Both CD8+ and CD4+ must recognize antigen on the same APC simultaneously

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111
Q

T or F: CD4+ cells can induce macrophages to up regulate B7 expression.

A

T

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112
Q

What must naive T cells do once they’re activated?

A

They must re-enter the cell cycle and divide rapidly, producing large numbers of progeny that will differentiate into “armed” effector T cells

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113
Q

The proliferation and differentiation of activated T cells is driven by ________.

A

IL-2

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114
Q

T or F: T cells can respond to both low and high concentrations of IL-2.

A

Kinda true, kinda false. T cells constitutively express a moderate affinity IL-2 receptor, and activation of a T cell induces expression of a high affinity form of IL-2 that allows T cells to respond to lower IL-2 concentrations

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115
Q

What is the structure of the high affinity IL-2 receptor?

A

It’s a heterodimer that consists of an alpha, a beta, and a gamma chain. All three chains traverse the membrane of the T cell

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116
Q

What is the structure of the moderate affinity IL-2 receptor?

A

Only composed of beta and gamma chains until the T cell is activated. Once activated, an alpha chain is expressed and the moderate affinity receptor becomes a high affinity receptor

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117
Q

What is an armed effector T cell and what differentiates them from naive T cells?

A

A T cell that can produce all of the proteins that are required for its specialized function

  • They don’t need costimulation signals
  • They express higher levels of LFA-1 and CD2, but lose L-selectin
  • They express VLA-4 that promotes movement into infection site
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118
Q

When to activated T cells differentiate into effector T cells?

A

After 4-5 days of rapid proliferation of the T cell clonal line

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119
Q

What are the 3 primary classes of effector T cells?

A
  1. Effector CD8 T cells
  2. Type I helper T cells
  3. Type II helper T cells
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120
Q

Type I helper T cells are primarily involved in ______.

A

The development of cell-mediated immune responses

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121
Q

What functions do cytokines produced by type I helper cells perform?

A
  1. Stimulate macrophages, making them more phagocytic and more bactericidal
  2. 2nd activation signal by helping B cells; influences class switching and somatic hypermutation
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122
Q

TH1 CD4 cells induce B cells to produce antibodies that are efficient for _______.

A

Opsonization – IgG1 and IgG3

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123
Q

Type II helper T cells are primarily involved in __________.

A

Development of humoral immune responses

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124
Q

TH2 CD4 cells induce B cells to produce which antibodies?

A

All the other isotypes that TH1 cells don’t induce (everything but IgG1 and IgG3)

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125
Q

T or F: Both TH1 and TH2 CD4 cells influence class switching and somatic hypermutation.

A

T

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126
Q

When CD4 cells leave the thymus they are considered _____ cells. The decision to become TH1 or TH2 occurs when ______.

A

TH0; Decision to become TH1 or TH2 occurs upon 1st encounter with antigen

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127
Q

Why is the decision between TH1 and TH2 CD4 cells important?

A

It determines whether the acquired immune response will be primarily cell-mediated or antibody-mediated

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128
Q

CD4 TH0 cells activated in the presence of ____ and _____ tend to become TH1 effector cells.

A

IL-12 and IFN-gamma

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129
Q

What cytokine inhibits the development of TH2 cells?

A

IFN-gamma

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130
Q

When is IL-12 produced?

A

It’s produced by macrophages and dendritic cells in response to viral and some intracellular bacterial infections

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131
Q

CD4 TH0 cells that are activated in the presence of _____ and _______ tend to differentiate into TH2 cells.

A

IL-4 and IL-6

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132
Q

Which cytokines inhibit the generation of TH1 cells?

A

IL-4 and IL-10

133
Q

NK T cells are possible sources of which cytokine?

A

IL-4

134
Q

TH2 cells produce ___ and ____ which inhibit activation and growth of TH1 cells.

A

IL-10 and TGF-beta

135
Q

TH0 cells that are presented with low concentrations of antigen that bind weakly to the TCR tend to differentiate into ____ cells.

A

TH2

136
Q

TH0 cells that are presented with high concentrations of antigen that bind tightly to the TCR tend to differentiate into ____ cells.

A

TH1

137
Q

Three ways for CD8 T cells to be activated

A
  1. Dendritic cells express high levels of B7 and can activate naive CD8 T cells.
  2. APC stimulates effector CD4 T cell, which in turn activates the APC. Then the activated APC expresses B7, which costimulates the naive CD8+ cell.
  3. APC activates CD4 T cell to make IL-2 and naive CD8 T cell to express IL-2 receptors. IL-2 secreted by CD4 is bound by CD8.
138
Q

Other than TH1 and TH2, what are other CD4+ effector cell types?

A

Treg, TH17, TH3

139
Q

What three characteristics to Tregs have?

A
  1. Self-antigen specific T cell receptors
  2. Express CD25 surface protein
  3. Express transcriptional repressor FoxP3
140
Q

TH0 cells differentiate into Treg cells when activated in presence of _____.

A

TGF-beta

141
Q

What is Immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX)? What’s the treatment?

A

Deficiency of FOXP3, which causes a fatal autoimmune disease directed at a variety of host tissues (gut, thyroid, pancreatic beta cells, skin). The only effective treatment is a bone marrow transplant from a healthy HLA-identical sibling.

142
Q

What are TH17 cells?

A

A subset of T helper cells that produce IL-17, IL-21, and IL-22. They’re thought to promote neutrophil influx into inflammatory sites and they produce cytokines that elicit antimicrobial protein production by epithelial cells.

143
Q

What can occur as a result of a deficiency of TH17 cells?

A

Patient can become susceptible to opportunistic pathogens

-TH17 cells have been implicated in several autoimmune diseases

144
Q

What are TH3 cells?

A

A new subset of helper T cells that produce TGF-beta and IL-10 and are thought to be involved in mucosal immunity and maintaining a non-inflammatory environment in the mucosa of the guy, preventing immune reactivity to non-pathogenic non-self antigens

145
Q

What cytokines drive differentiation of TH0 cells to TH3 cells?

A

TGF-beta, IL-4, and IL-10

146
Q

B7 is unregulated in ____ cells in response to potential infection.

A

APCs

147
Q

What activation stimuli do armed effector T cells require? How is this different from naive T cells?

A

Binding of TCR to specific peptide antigen:MHC complex. Naive T cells also require a co-stimulatory signal.

148
Q

What is an armed effector T cell?

A

A fully differentiated T cell that is ready to perform its effector function

149
Q

What are the main types of effector T cells?

A

CD8+ effector T cells, CD4+ helper T cells (TH1 and TH2)

150
Q

T or F: Naive T cells do not express the adhesion molecules (VLA-4) required for entry into inflammatory sites.

A

T: because naive T cells have no effector functions

151
Q

_________ cells down-regulate L-selectin expression, which prevents them from entering secondary lymphoid tissues via HEVs.

A

Effector CD8+ T cells (CTLs)

152
Q

T or F: Effector CD8+ T cells up regulate VLA-4 expression.

A

T: This allows them to bind to vascular endothelium at sites of inflammation

153
Q

Why shouldn’t effector CD8+ T cells enter secondary lymphoid tissues?

A
  1. They have no role there

2. If they entered they could attack APCs that present their specific peptide antigen

154
Q

Effector CD8+ T cells up regulate expression of _____ and _____, which initiate interactions between the effector T cells with their potential target cells.

A

Cell adhesion molecules: LFA-1, CD44, and CD2

155
Q

What are the principal effector molecules of CTLs?

A

Cytotoxins (perforin, granzymes, granulysin)

156
Q

What are the primary effector molecules for CD4 T cells?

A

Cytokines

157
Q

TH1 cells produce cytokines that _______.

A

Upregulate macrophage functions and generally promote cell-mediated immunity

158
Q

What are the cytokines for CD8 T cells?

A

IFN-gamma and LT

159
Q

What are the cytokines for TH1 cells?

A

IFN-gamma, GM-CSF, TNF-alpha, LT, IL-3

160
Q

What are the cytokines for TH2 cells?

A

IL-4, IL-5, IL-10, IL-13, TGF-beta

161
Q

TH2 cells produce cytokines that _______.

A

Generally promote humoral immune responses

162
Q

Which cytokine has anti-viral properties and inhibitys TH2 cell development?

A

IFN-gamma

163
Q

T or F: CTLs express Fas ligand.

A

T: Fas ligand helps induce apoptosis

164
Q

What is perforin?

A

A cytotoxin that polymerizes with other performs to form a pore in the membrane of a target cell. It aids in delivering contents of granules into the cytoplasm of the target cell.

165
Q

What is granulysin?

A

A detergent like protein that associates with cellular membranes and helps form pores in membranes. It has antimicrobial actions and can induce apoptosis.

166
Q

What are granzymes?

A

Molecules that associate with the perforin-mediated pore and are brought along with the portion of the membrane they associate with as part of endocytosis (“reparative endocytosis” is the new model)

167
Q

What transcription factors are associated with Treg cells?

A

FOXP3

168
Q

What transcription factors are associated with TH1 cells?

A

T-bet

169
Q

What transcription factors are associated with TH2 cells?

A

GATA-3

170
Q

What do the cytokines in CTLs do?

A

They stimulate cells to up regular expression of proteins involved in antigen presentation, increasing the chance that an infected cell will be recognized by an effector CTL

171
Q

T or F: In many cases, neighboring cells are killed by CTLs along with cells that bear the CTL’s cognate antigen.

A

F: neighboring cells are spared

172
Q

What ensures that CTLs focus on their target cells and not neighboring cells?

A

Polarization of CTLs when their TCR is bound to MHC:peptide complexes

173
Q

______ are serene proteases that initiate the programmed cell death pathway.

A

Granzymes

174
Q

All apoptosis initiators lead to the activation of a series of cysteine proteases known as ______.

A

Caspases

175
Q

What are the steps of Fas-mediated apoptosis?

A
  1. FasL homotrimer binds to Fas, inducing trimerization of Fas and brining the death domains of Fas together
  2. Adaptor proteins (also containing death domains) bind to death domains of the Fas trimer
  3. Cascade of caspase activity is initiated, which activates CAD (caspase activatable DNase)
  4. Activated CAD enters the nucleus and cleaves the chromosomal DNA, killing the cell
176
Q

What signals do macrophages require to be activated and what cells deliver these signals?

A
  1. IFN-gamma
  2. CD40 ligand on the T cell interacts with CD40 on the macrophage
    Both signals can be delivered by TH1 cells
177
Q

Activation of a macrophage leads to what biochemical responses by the macrophage? (5)

A
  1. Upregulation of phagosome-to-lysosome fusion
  2. Production of NO and oxygen radicals
  3. Production of antibacterial peptides and proteases
  4. Upregulation of MHC class II, B7, and CD40
  5. Production of IL-12, which stimulates differentiation of TH0 cells into TH1 cells
178
Q

Th1 produces IFN-gamma and CD40, which ______.

A

Activate macrophages and make them more bacteriocidal

179
Q

TH1 produces TNF-beta and Fas ligand, which _______.

A

Can induce a chronically-infected macrophage to undergo apoptosis

180
Q

TH1 cells produce IL-2, which _______.

A

Is a growth factor for T cells and can assist in the activation/proliferation of naive CD8+ T cells

181
Q

TH1 cells produce IL-3 and GM-CSF, which _____.

A

Induce macrophage differentiation in the bone marrow

182
Q

TH1 cells produce lymphotoxin (LT) and TNF-alpha, which _____.

A

Facilitate macrophage binding to epithelium/exit from blood vessels at sites of infection (diapedesis)

183
Q

TH1 cells produce macrophage cemotactic factor, (CXCL2) which _______.

A

Causes macrophages to accumulate at sites of infection

184
Q

What will an effector TH cell do if it recognizes its cognate peptide antigen:MHC complex on the surface of a B cell?

A

It will supply the second signal of activation (production of cytokines and CD40 ligand) to the B cell

185
Q

Effector TH1 cells produce cytokines that stimulate B cell activation and differentiation into cells that produce antigen-specific Abs of ______ isotypes. What are these isotypes important for?

A

IgG1 and IgG3– important opsonizing antibodies

186
Q

Effector TH2 cells produce cytokines that stimulate B cell activation and differentiation into cells that produce antigen-specific Abs of ______ isotypes. What are these isotypes important for?

A

IgG2, IgG4, IgA, and IgE – important for neutralization and complement fixation

187
Q

What effect does IL-2 have on T cells?

A

Effects T cell growth

188
Q

What effect does IFN-gamma have on macrophages?

A

It activates them and up-regulates MHC class I and II

189
Q

What effect does lymphotoxin have on macrophages?

A

It activates them and induces NO production

190
Q

What effect does IL-4 have on B cells?

A

Activation and increased MHC class II induction

191
Q

What effect does IL-4 have on T cells?

A

Assists in growth and survival

192
Q

What effect does IL-3 have on hematopoietic cells?

A

It’s a growth factor for progenitor hematopoietic cells

193
Q

What effect does TNF-alpha have on macrophages?

A

It activates them and induces NO production

194
Q

What effect does GM-CSF have on hematopoietic cells?

A

It increases the production of granulocytes, macrophages, and dendritic cells

195
Q

When do granulomas form?

A

When microbes resist destruction by macrophages; prevents dissemination of microbes

196
Q

What are the steps of signaling through cytokine receptors?

A
  1. Cytokine receptors have at least two chains whose cytoplasmic domains bind JAKs
  2. Cytokine binding dimerizes the receptors, bringing the JAKs together, phosphorylating and activating them
  3. STATs (transcription factors) bind to the phosphorylated receptors and are phosphorylated by the JAKs
  4. Phosphorylated STATs form dimers that move into the nucleus to initiate gene transcription
197
Q

What characteristics do the most efficient antibodies possess?

A
  1. Produced early in infection
  2. Bind antigen with high affinity
  3. Antibodies are more effective as the immune response progresses
198
Q

When does the onset of antibody occur after infection?

A

Usually about a week after infection

199
Q

Upon binding to antigen, what do surface IgM molecules do?

A

They become physically cross linked to each other and are drawn into the localized area of contact with the antigen, which results in signaling to the inside of the cell

200
Q

T or F: Antibodies themselves are not toxic or destructive to pathogens.

A

T

201
Q

What is the signal transduction unit for the BCR?

A

Ig-alpha/Ig-beta complex

202
Q

_______ is the B cell co-receptor?

A

CR2 (complement receptor 2)

203
Q

What do the ITAMs on the tails of Ig-alpha and Ig-beta on the BCR do?

A

When the ITAMs become clustered due to receptor cross linking, tyrosines within the ITAMs become phosphorylated, tyrosine kinases are activated, and intracellular signaling pathways are initiated

204
Q

What happens when the B cell co-receptor (CR2) is engaged?

A
  1. The cytoplasmic tail of CD19 becomes phosphorylated
  2. CD19 can bind to intracellular signaling molecules
  3. Signals are generated that synergies with signals generated by the BCR complex, majorly amplifying the signaling
205
Q

T or F: Signaling through the BCR in combination with signaling through the B cell co-receptor sufficient to induce activation of the naive B cell.

A

F: still need a second signal of activation from helper T cells

206
Q

What are TD antigens?

A

Antigens that require help from an antigen-activated effector CD4+ T cell

207
Q

What are TI antigens?

A

Antigens that can activate B cells in absence of T cell help

208
Q

How can TI antigens overcome the need for T cell help?

A
  1. Mitogens (TI-1 antigens) have intrinsic capacity for inducing B cell proliferation by engaging the BCR and PRRs
  2. TI-2 antigens act by heavily cross linking BCRs on the surface of the B cell
209
Q

T or F: At high concentrations TI-1 antigens can activate almost any B cell, regardless of BCR specificity.

A

T

210
Q

What are the limitations of TI-1 antigens?

A

They primarily produce IgM antibodies and there is no affinity maturation or differentiation to memory cells

211
Q

What are TI-2 antigens typically composed of and how do they act?

A
  • Composed of repetitive carbohydrate or protein epitopes present at high density on the surface of a microorganism
  • Act by densely cross linking BCRs and B cell co-receptors to where no other signals are needed
212
Q

_______ antibodies can be induced by TI-2 antigens.

A

IgM and IgG

213
Q

What are the limitations of TI-2 antigens?

A
  1. No significant isotype switching
  2. No affinity maturation
  3. No immunological memory is provided
214
Q

TI-2 antigens are responded to primarily by _____.

A

B1 B cells

215
Q

How does antigen enter the secondary lymphoid tissues and where does it enter?

A

Via the lymph; enters draining lymph node nearest the infected tissue

216
Q

What 2 roles does the BCR play in B cell activation?

A
  1. Binding to cognate antigen
  2. Internalizing the antigen (so that it can be processed) and peptides presented on MHC class II molecules on the B cell surface
217
Q

A B cell that receives the 2nd signal of activation from an effector CD4+ cell will form a focus of dividing ________ within the T cell zone of the secondary lymphoid tissue.

A

Lymphoblasts

218
Q

Which cytokines help B lymphoblasts differentiate into plasma cells?

A

IL-5 and IL-6

219
Q

T or F: There is no isotype switching in the primary focus within the T cell zone.

A

F: There is some isotype switching, but mostly IgM is secreted

220
Q

What are centroblasts?

A

Centroblasts are lymphoblasts from the primary focus that migrate to the primary follicles with their helper T cells, where their rate of division increases a lot

221
Q

What happens in the follicle of secondary lymphoid tissue as the number of centroblasts rapidly expands?

A

The follicle changes and becomes dominated by the germinal center, which contains newly formed B cells

222
Q

When do germinal centers appear in lymph nodes?

A

About one week after the start of infection– they’re responsible for the swelling of lymph nodes!

223
Q

Where do the vast majority of lymphocytes within the germinal center come from?

A

The majority are clones derived from one or a few of the founder pairs of antigen-activated B and T cells

224
Q

T or F: The B cells that are present in follicles before entry of the activated B cell-T cell conjugates are pushed to the outside of the germinal center.

A

T

225
Q

T or F: Affinity maturation occurs in centrocytes during the germinal center reaction.

A

T

226
Q

Centroblasts give rise to slower dividing cells that express Ig with a wide range of antigen affinities, known as _____.

A

Centrocytes

227
Q

In a germinal center reaction, centrocytes are programmed to undergo apoptosis unless they receive survival signals. What delivers these survival signals?

A

Helper T cells produce CD40L, which binds to CD40 on the centrocyte

228
Q

What must occur for a centrocyte to engage a helper T cell and prevent apoptosis?

A

The centrocyte must have successfully competed with other centrocytes for antigen that it then internalized, processed, and presented peptides to the cognate T cell.

229
Q

What cells remove centrocytes from the germinal center for apoptosis?

A

Tingible body macrophages

230
Q

T or F: Somatic hypermutation can give rise to self-reactive B cells within the germinal center.

A

T: When a centrocyte acquires a self-reactive BCR, it should no longer have specificity for the original antigen and will be unable to compete for binding to antigen on FDCs. These cells don’t receive survival signals and will die.

231
Q

What are follicular dendritic cells (FDCs)?

A

Stromal cells of primary lymphoid follicles that pick up antigen and display it on their surface for long periods of time (they don’t internalize antigen)

232
Q

T or F: FDCs interact with one B cell at a time.

A

F: they have many long processes and are able to interact with many B cells simultaneously

233
Q

How are FDCs different from the dendritic cells that present peptide antigens to T cells?

A

FDCs aren’t derived from hematopoietic stem cells and they don’t express MHC class II molecules. Instead, they express Fc receptors and complement receptors on their surface, and they use these to capture immune complexes.

234
Q

What are iccosomes (immune-complex coated bodies)?

A

Bundles of membrane coated with immune complexes that bud off of FDCs (like lil beads on a string)

235
Q

What happens to B cells that survive the selection process in the germinal center?

A

They continue to proliferate and begin to differentiate into plasma cells, that then leave the secondary lymphoid tissue and migrate to bone marrow or Peyer’s patches in the gut

236
Q

T or F: At the height of the adaptive immune response, most B cell differentiation is into plasma cells.

A

T: to satisfy the need for large quantities of antigen-specific antibodies

237
Q

T or F: In the later stages of a successful immune response, B cells within the germinal center differentiate primarily into plasma cells.

A

F: Memory B cells

238
Q

IL-5 strongly promotes class switching to _____.

A

IgA

239
Q

IL-4 strongly promotes class switching to ____.

A

IgE

240
Q

In what tissues is IgG primarily found?

A

Extracellular spaces and serum

241
Q

In what tissues is IgM primarily found?

A

Blood

242
Q

In what tissues is IgA primarily found?

A

Mucosal secretions and serum

243
Q

In what tissues is IgE primarily found?

A

Bound to the high-affinity FCERI receptor on mast cells in the skin and in the linings of the GALT and BALT

244
Q

The process of isotype switching maintains antigen-specificity of the antibody while altering _______.

A

The Fc region of the heavy chain (constant region)

245
Q

What are the 3 critical functions of the Fc regions of antibody molecules?

A
  1. Delivery of Ab to sites within the body that would otherwise be inaccessible
  2. Some isotypes of Ab have ligands in the Fc region that can bind the C1 complement component and initiate the classical complement cascade
  3. Recruitment of non-specific effector cells (macrophages, NK cells, mast cells, granulocytes)
246
Q

T or F: Fc regions of antibodies form a bridge between the innate and acquired arms of the immune response.

A

T

247
Q

_____ is the most abundant and most important antibody isotype for control of most infections. Why?

A

IgG

1) it can fix complement
2) most phagocytes as well as NK cells have Fc receptors that recognize the Fc portion of IgG molecules
3) it’s actively transported into EC spaces
4. It has the longest half-life of the isotypes

248
Q

What benefit does the pentameric structure of IgM provide? What consequence

A

Benefit: IgM can bind to microorganisms/antigens with very high avidity
Consequence: Large size limits its ability to move into inflammatory sites

249
Q

Which Ig isotypes protect blood and EC fluids?

A

IgG, IgM, and IgA

250
Q

T or F: IgM can activate the complement cascade.

A

True dat

251
Q

What is septicemia and what can prevent/control it?

A

Septicemia is blood-borne infection, IgM, IgG, and IgA can help control it

252
Q

Where do IgA-producing plasma cells primarily reside?

A

In patches of mucosal-associated lymphoid tissues in the lamina propria

253
Q

What does the poly-Ig receptor do?

A

It sits on the basolateral surface of epithelial cells and binds polymeric Igs (especially IgA). It then transports Igs across epithelium via transcytosis.

254
Q

What is transcytosis?

A

Transport of molecules from one side of an epithelium to the other by endocytosis into vesicles within the epithelial cells at one face of the epithelium and release of vesicles at the other

255
Q

What is FcRn (Brambell receptor)?

A

An Fc receptor present on vascular endothelial cells that actively transports IgG from the blood into extracellular spaces (1 IgG per 2 copies of the Brambell receptor)

256
Q

________ is responsible for transporting IgG across the placental barrier into fetal circulation.

A

Brambell receptor

257
Q

What’s involved in the passive transfer of immunity from mother to child?

A

IgG is passed from the mother to the developing fetus

IgA is in breast milk

258
Q

Low affinity Fc receptors bind to __________.

A

Antibody that is bound to its specific antigen

259
Q

T or F: NK cell activity cannot be enhanced by immunization.

A

T

260
Q

T or F: NK cells recognize specific antigens.

A

F

261
Q

____ and _____ act on NK cells to elicit production of IFN-gamma, which then plays a role in amplification of inflammatory reactions.

A

TNF-alpha and IL-12

262
Q

______ cells produce IL-1 and GM-CSF, which modulate macrophage activity and have pro inflammatory effects.

A

Activated NK cells

263
Q

______ are the effectors of ADCC (antibody dependent cell-mediated cytotoxicity).

A

NK cells

264
Q

What does the FCgammaRIII receptor do?

A

It can bind to IgG that is bound to infected host cells, causing the NK cell to degranulate. This initiates apoptosis of the infected host cell.

265
Q

How do NK cells serve as a bridge between innate and acquired immunity?

A

They don’t express antigen-specific receptors, but they can initiate killing of cells that have been recognized as infected by specific antibody molecules

266
Q

T or F: ADCC by NK cells depends on the MHC class I inhibitory signal.

A

F

267
Q

T or F: Mast cells do not make any antigen-specific receptor molecules.

A

T: but they do hi-jack an array of antigen-specific receptors that are produced on B cells

268
Q

What is the FcERI receptor?

A

A high-affinity Fc receptor expressed by mast cells and eosinophils; it binds to the Fc portion of IgE antibodies

269
Q

T or F: There is a lot of IgE floating in the serum.

A

F: most IgE produced by B cells is rapidly bound to FcERI receptors

270
Q

What is the role of mast cells?

A

Initiate inflammatory responses in epithelial tissues in response to antigens that have previously initiated an antigen-specific IgE antibody response

271
Q

What induces a mast cell to release its granule content?

A

Crosslinking of antigen-specific IgE bound to FcERI receptors by specific antigen

272
Q

What is the purpose of the complement cascade?

A

It marks foreign material for destruction and removal by covalently binding opsonins to the surface of the foreign material

273
Q

What are the three pathways of the complement cascade?

A
  1. Classical
  2. Lectin
  3. Alternative
274
Q

Which complement cascade pathway is an example of bridging between the acquired and innate immune response?

A

Classical pathway

275
Q

What triggers the classical pathway of the complement cascade?

A

Antibody bound to the surface of the microbe

276
Q

What triggers the alternative pathway of the complement cascade?

A

Direct recognition of certain microbial structures

277
Q

T or F: The alternative and lectin pathways of the complement cascade are purely innate mechanisms.

A

T

278
Q

What triggers the lectin pathway of the complement cascade?

A

Mannose-binding lectin binding to terminal mannose residues on microbial glycoproteins and glycolipids

279
Q

Where are complement proteins synthesized?

A

In the liver in inactive (zymogen) form

280
Q

Complement proteins are activated by proteolytic cleavage, which results in _____.

A

A larger enzymatically active component

A smaller fragment that often has an inflammatory effect (anaphylatoxin)

281
Q

How is complement opsonization different from Ab-mediated opsonization?

A

Complement opsonization is permanent (covalently bound)

282
Q

What are anaphylatoxins?

A

Complement fragments that recruit fluid and inflammatory cells to sites of antigen deposition.

283
Q

______ is a powerful and important chemotactic factor for neutrophils.

A

C5a

284
Q

Which complement fragments can activate vascular epithelium, resulting in leaking of fluids from the vascular into the surrounding tissues.

A

C3a, C4a, C5a

285
Q

What does C3b do?

A
  • It serves as a potent opsonin, facilitating uptake and destruction of the pathogen
  • It is also a component of the C5 convertase enzyme that is required for activation of the membrane attack complex
286
Q

_____ is the most important and most abundant of the complement proteins.

A

C3

287
Q

All three complement pathways are dependent on the formation of ______.

A

C3 convertase

288
Q

The classical C3 convertase is composed of what? How about the alternative C3 convertase?

A

Classical: C2a and C4b
Alternative: Bb and C3b

289
Q

How does the lectin pathway of complement activation work?

A
  1. MBP binds to terminal mannose residues on the surface of bacteria
  2. MBP binds to MASP-1 and MASP-2, which become activated and are able to cleave C4 to form C4a and C4b and C2 to form C2a and C2b
  3. C2b and C4b come together to form the C3 convertase, which cleaves C3 to form C3a and C3b
  4. Then everything is the same as the classical pathway
290
Q

What is C1 composed of?

A
  1. C1q (a large molecule that binds to Fc region of antibody molecules)
  2. C1r: inactive serine protease that cleaves itself when C1q binds to Ab
  3. C1s: inactive serine protease that is activated upon C1r cleavage and cleaves complement components C4 and C2
291
Q

C1 is inactive until _______.

A

Until it’s bound to the Fc region of Ab

292
Q

Which immunoglobulins can fix complement?

A

IgM > IgG > IgA

293
Q

How does the classical pathway of complement activation work?

A
  1. C1 binds to the Fc region of an Ab that is bound to its specific antigen (via C1q)
  2. C1r cleaves itself then cleaves C1s
  3. Activated C1s cleaves inactive C2 and C4, forming C2b and C4b, which can bind to the microbial surface and form C3 convertase
294
Q

How is the membrane attack complex formed?

A
  1. C5 convertase cleaves C5, forming C5a and C5b
  2. C5b binds to C6 and C7, and the complex binds to the membrane via C7
  3. C8 binds to the complex and inserts into the cell membrane
  4. 10-15 C9 molecules bind to form a pore in the membrane
  5. The pore causes osmotic disintegrate and death of the bacterium or RBC
295
Q

What makes up C5 convertase in the classical and alternative pathways?

A

Classical: C4b, C2a, C3b
Alternative: C3b2, Bb

296
Q

T or F: The C5a fragment is a vasoactivator and an important chemokine for neutrophils.

A

T

297
Q

When do deficiencies in membrane attack complex components result in susceptibility?

A

Only in Neisseria, showing that the function of the complement system doesn’t have a huge role in host defense

298
Q

What is Leiner disease?

A

A disease resulting from deficiency of C5. Symptoms: seborrheic dermatitis, diarrhea, recurrent local and systemic infection, CNS problems, and failure to thriveq

299
Q

What prevents C4b and C2a from binding to “self” cellular components, marking them for destruction by phagocytes?

A

C4b and C2a are only able to bind to structures immediately adjacent to the bound antibody molecule, and complement control proteins deactivate C3b that has been deposited on host cells.

300
Q

Phagocytes have ____ that bind to C3b, which encourages the phagocytes to remove foreign material via phagocytosis.

A

CR1 (complement receptors)

301
Q

T or F: C3 convertase of the alternative pathway can amplify the amount of C3 deposition that results from the classical pathway.

A

T

302
Q

In dealing with the complement cascade, factor B deficiency results in ___________.

A

Total lack of alternative complement activation as well as significantly reduced C3b deposition following either lectin or classical pathway activation

303
Q

How does the alternative pathway of complement activation work?

A
  1. C3 is cleaved to produce C3b and C3a
  2. C3b binds to pathogen and serves as a ligand for factor B binding
  3. C3b/B complex is susceptible for cleavage by factor D, which cleaves B into Bb and Ba
  4. Bb stays complexed to C3b and this is the C3 convertase of the alternative pathway
  5. The rest of the pathway works like the classical pathway
304
Q

On what cells is CR1 expressed and what does it bind to?

A

APCs (macrophages, neutrophils, B cells, dendritic cells)

Binds to C3b and C4b

305
Q

T or F: C3b/CR1 interaction initiates phagocytosis/respiratory burst.

A

F: Not by itself. It acts with IgG/Fc-gamma receptor or IFN-gamma signaling to initiate phagocytosis/respiratory burst

306
Q

On what cells is CR2 expressed and what does it bind to?

A

B cells and follicular dendritic cells

Binds to C3d, C3dg, iC3b, and Eptein-Barr virus

307
Q

T or F: CR2 is a component of the B cell coreceptor.

A

T

308
Q

On what cells are CR3 and CR4 expressed and what do they bind to?

A

Macrophages and neutrophils

Bind to iC3b

309
Q

T or F: CR3/iC3b binding is sufficient to activate phagocytosis.

A

F

310
Q

Why is it significant that eryhtrocytes bear CR1 receptors?

A

Most immune complexes in circulation are bound to erythrocytes. When erythrocytes circulate through the spliver, tissue macrophages remove and degrade immune complexes by binding to C3b via their CR1 receptors.

311
Q

What are podocytes?

A

Specialized epithelial cells that express CR1 and cover the capillaries within the kidney glomeruli. They help remove and dispose of immune complexes that cross basement membranes of capillaries.

312
Q

What is systemic lupus erythmatosis (SLE)?

A

An immune complex disease that can result in eventual failure of the kidney. Happens because podocytes are overwhelmed and the kidney glomeruli are damaged.

313
Q

What are characteristics of anaphylatoxins?

A
  • Induce smooth muscle contraction
  • Have vasoactive effects on local blood vessels (increasing blood flow)
  • Induce mast cell/basophil degranulation
  • Facilitate imitation of acquired immune responses
314
Q

What does C5a anaphylatoxin act on?

A
  • Acts directly on neutrophils and monocytes, increasing their adherence to blood vessel walls and acting as a chematractant
  • Upregulates phagocytosis, CR1, and CR3 expression
315
Q

How is the complement cascade passively regulated?

A

After cleavage, thioester bonds are rapidly hydrolyzed

316
Q

How is the complement cascade actively regulated?

A
  1. Plasma (soluble) regulatory proteins

2. Cell-surface associated proteins

317
Q

What does C1 inhibitor (C1INH) do?

A
  • Binds to activated C1r:C1s, causing them to dissociate from C1q and limiting the time C1 is enzymatically active
  • Inhibits a plasma protease involved in the production of bradykinin
318
Q

What is hereditary angioneurotic edema (HANE) and what is the Tx?

A

Disease involving a deficiency of C1INH production. It results in an excess of cleaved C4a and C2b fragments. C2b is further cleaved to form C2 kinin, which causes edema (swollen lips, etc). Treatment: C1INH replacement therapy

319
Q

What does C4BP do?

A

It binds to C4b and displaces the C2b fragment, deactivating the C3 convertase and rendering C4b as susceptible to cleavage/inactivation by factor I.

320
Q

What does factor H do?

A

Binds to C3b and makes it susceptible to cleavage/inactivation by factor I, with the formation of iC3b.

321
Q

What does factor I do?

A

It inactivates C3b and C4b.

322
Q

What happens in factor I deficiency?

A

It leads to depletion of C3 and prevents formation of iC3b, which is a critical opsonin in the absence of antibody.
-Patients are more susceptible to ear infections and abscesses caused by pyogenic bacteria

323
Q

What does decay-accelerating factor (DAF) do?

A

Binds to C4b and C3b components of the C3b converses, causing their dissociation and inactivation

324
Q

What does membrane co-factor protein (MCP) do?

A

Binds to B4b and C3b, making them susceptible to cleavage/inactivation by factor I

325
Q

What does CD59 (protection) do?

A

Binds to the C5b,6,7,8 complex and prevents polymerization of C9 in the membrane, ultimately preventing pore formation

326
Q

T or F: CD59 effectively prevents formation of the membrane attack complex on host cells and pathogens.

A

F: Prevents formation of MAC on host cells but doesn’t inhibit MAC formation on pathogen surface

327
Q

_____ and ____ are linked to the plasma membrane via the phosphoinositol glycolipid tail.

A

CD59 and DAF

328
Q

What is paroxysmal nocturnal hemoglobinuria?

A

Disease in patients that lack the phosphoinositol glycolipid tail and are deficient in CD59 and DAF. Symptom: episodes of intravascular RBC lysis.

Immunology (3 decks)

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