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Year 1 MCD > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the function of the immune system?

A

To protect the host from pathogenic microbes by distinguishing self from non-self, and recognising danger signals.

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2
Q

What general balance does the immune system need to negotiate?

A

A balance between clearing the pathogen and collateral damage to the host (immunopathology)

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3
Q

How does the immune system keep up with the evolutionary arms race?

A

It is flexible and has a rapid immune response. Our most polymorphic genes control the immune system (HLA and KIR).

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4
Q

What is the primary response against a virus? What purpose does this serve?

A

Spike of type-1 interferon, followed by a peak of NK cells. It works to bring down virus titre.

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5
Q

What are the two TYPES of immune response?

A

Innate and Acquired

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6
Q

What are the anatomical and physiological barriers of the innate immune system?

A

Anatomical: Skin, Mucus, Cilia
Physiological: pH, lysozyme, interferons, antimicrobial peptides, complement

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7
Q

What are the components of the innate immune system?

A

Cellular: Neutrophils, NK Cells, Macrophages (and monocytes), Dendritic cells, Mast cells and the Granulocytes
Humoral: Anti-microbial peptides, complement and cytokines

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8
Q

What are the components of the adaptive/acquired immune system?

A

Cellular: Macrophages (and monocytes), Dendritic cells, Mast cells and Lymphocytes
Humoral: Complement, Cytokines and Antibodies

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9
Q

How is the innate response triggered?

A

PAMPs (pattern-associated molecular patterns) and DAMPs (danger-associated molecular patterns)

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10
Q

What are the pattern-recognition receptors?

A

Extracellular: Toll-like receptors
Intracellular: Nod-like receptors, AIM2, RGI-I like receptors

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11
Q

What are the functions of the innate immune system?

A
  • destroy invading nucleic acids
  • activates interleukins to activate inflammatory pathways
  • elicits type-1 interferons
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12
Q

What does the acute phase inflammatory response involve?

A
  • Production of acute phase proteins by the liver. These include C-reactive protein and serum amyloid protein to bind to molecules on cell walls, and mannan-binding lectin, binding to mannase sugar. These molecules direct phagocytes to identify and ingest the infectious agent.
  • fever response caused by interleukin-1
  • increased production of white blood cells
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13
Q

What are cytokines?

A

Large family of small proteins that carry messages from one cell to another.

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14
Q

What are the Granulocytes and their functions?

A

Basophils: release histamines, serotonin and prostaglandins
Neutrophils: phagocytic
Eosinophils: work against parasites

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15
Q

What is an antigen?

A

A molecule that reacts with antibodies or a T-cell

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16
Q

What is an immunogen?

A

An antigen that can initiate and immune response

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17
Q

What is an antibody?

A

An immunoglobulin molecule in blood and bodily fluids which binds specifically to an antigen.

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18
Q

What are the different classes of immunoglobulins and their relative percentages in serum?

A 
IgG (75%)
IgM (10%)
IgA (?)
IgE (?)
IgD (?)
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19
Q

How dies an antibody recognise an antigen?

A

The antibody’s binding site makes a perfect fit with an epitope on the antigen.

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20
Q

How can an antibody help eliminate a virus?

A
  • Neutralisation (binds to virus, preventing attachment to cell)
  • Opsonisation (virus-antibody complex is phagocytosed)
  • Complement mediated lysis of enveloped virus
  • Antibody-dependent cell-mediated cytotoxicity (ADCC)
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21
Q

What are the granular and agranular leukocytes?

A

Granular: NK, monocytes and granulocytes
Agranular: lymphocytes

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22
Q

What is the difference between active and passive immunity?

A

Active immunity is acquired immunity after infection. Passive immunity is acquired without needing to activate the immune system.

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23
Q

What antigens do BCR and TCR recognise?

A

BCR recognises intact antigens

TCR recognises processed antigens presented on MHC molecules.

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24
Q

Where (genetically) do lymphocyte genetic recombinations occur?

A

On immunoglobulin gene segments (for B-cell) and TCR gene segments (for T-cell)

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25
Q

Where do T-lymphocytes meet antigens?

A

Antigen-presneting cells transport antigens to the secondary lymphoid tissues.

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26
Q

What are the professional antigen-presenting cells?

A
  • Dendritic cells
  • Macrophages
  • B lymphocytes
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27
Q

What are lymphoid organs?

A

Organised tissue in which lymphocytes interact with non-lymphoid cells.

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28
Q

What are the primary lymphoid organs?

A

Where lymphocytes are produced: Thymus and Bone marrow

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29
Q

What are the secondary lymphoid organs?

A

Where lymphocytes can interact with antigens: Lymph nodes, Spleen and MALT

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30
Q

What are the lymphatic vessels?

A

Venules, Veins and Ducts

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31
Q

What are the lymphatic tissues?

A

Nodules, Nodes and Tonsils and Peyer’s patches

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32
Q

How does the thymus change during infections and through ageing?

A

No obvious change during infections. Thymus output declines with age, but total number of lymphocytes do not.

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33
Q

How does bone marrow change during infections and through ageing?

A

Increased white cell production during infections. As we age, the bone marrow becomes less cellular but more fatty.

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34
Q

What are the different compartments in lymph nodes?

A

Lymphoid follicles are cortical to the T-cell areas. Germinal centers can exist on the lymphoid follicles during B-cell proliferation.

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35
Q

How is the organisation and segregation of lymphocytes in secondary lymphoid tissue achieved?

A

Through chemokine gradients.

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36
Q

What is the immunological role of the spleen?

A

Filters the blood for antigens.

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37
Q

What are the different compartments of the spleen?

A

Red pulp.

White pulp, made of periarterial lymphatic sheath (T-cell area), primary folicle (B-cell area) and germinal centers.

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38
Q

What are people without a spleen particularly susceptible to?

A

Infections with encapsulated bacteria.

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39
Q

How is the epithelium immunologically guarded?

A

Cutaneous immune system and Mucousal Associated Lymphoid Tissue (MALT).

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40
Q

What are the lymphoid tissues in the gut called?

A

Peyer’s patches.

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41
Q

What makes up MALT?

A

Peyer’s patches and M cells (dendritic cells of the gut).

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42
Q

How are antigens surveyed in the gut?

A

M cells sample the contents of the guts for antigens and uptake any antigens, traveling to lymphocytes in Peyer’s patches.

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43
Q

What makes up the cutaneous immune system?

A

Keratinocytes (physical barrier), Intraepidermal lymphocytes and Epidermal langerhan cells (similar function to M cells)

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44
Q

How does the body ensure the antigen meets with the specific lymphocyte?

A
  • Anatomical structure of the immune system

- Lymphocyte re-circulation

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45
Q

When do naive lymphocytes stop circulating?

A

When they are activated or die.

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46
Q

What is the name of the process by which cells extravasate?

A

Diapedesis

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47
Q

How do leukocytes extravasate into tissue?

A

1) Rolling: lymphocytes roll across the endothelial wall. Selecting binds the cell to the endothelium. The selections can be expressed on the endothelium or the cell.
2) Activation: cytokines attract the cell closer to the endothelium, allowing integrins to be activated.
3) Adhesion: Integrins change from a low-affinity state to a high-affinity conformation, allowing the cell to migrate into the tissue.

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48
Q

What does CD stand for?

A

Cluster of Differentiation

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49
Q

What are the features of lymphocytes under a microscope?

A

Large nucleus and granular cytoplasm

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50
Q

What receptors are found on T-cells?

A

All T-cells have CD3. There are two type of TCR: 90% are (alpha)(beta), 10% are (gamma)(delta).
2/3 of (alpha)(beta) are CD4, 1/3 are CD8

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51
Q

What receptors are found on B-cells? (excluding BCR)

A

CD19 and CD20

Can also express MHC Class II

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52
Q

What do follicular dendritic cells do?

A

Capture antigens to develop B-cells in germinal enters in lymph nodes.

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53
Q

How can the innate immune system recognise pathogens?

A

1) Detecting PAMPs
2) Detecting DAMPs
3) Detecting missing self (NK cells) using MHC Class I

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54
Q

Give examples of bacterial, viral, fungal and parasitic PAMPs

A

Bacterial: Flagellin, LPS, Peptidoglycans, Lipoteichoic Acid, Formyl peptides, DNA, Glycolypids
Viral: Envelope glycoprotein, ssRNA, dsRNA, Unmethylated CpG motifs.
Fungal: Mannoproteins, beta-glucans, Unmethylated CpG motifs, popspholipomannan
Parasite: Profilin, Glycolipids, DNA

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55
Q

Give examples of DAMPs from necrosis and injury

A

Necrosis: High ATP and DNA outside cells, Interleukin-1alpha, Interleukin 18, HSPs, S100 proteins
Injury: fragments from ECM such as Heparin sulphate, Hyaluronan, Aggrecan, Fibronectin, Collagens and Fibromodulin.

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56
Q

What are the properties of neutrophils?

A

They are polymorphonuclear leukocytes.
Short-lived
Migrate into tissue
First cells to be recruited to a site of tissue damage/infection
Have a multi-libed nucleus
Have primary azurophilic granules and secondary granules

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57
Q

How do neutrophils fight infection?

A

1) Move into tissue
2) Bind to pathogens. More effective after opsonisation as they have receptor proteins for opsonins.
3) Kill pathogen after phagocytosis.
4) Form NETs (neutrophil extracellular traps) by releasing granule proteins and chromatin to form extracellular fibres.

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58
Q

What are the two main types of opsonins?

A

Antibodies and complement

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59
Q

How do neutrophils kill phagocytosed bacteria?

A

Oxygen-independent:
- enzymes
- lysozyme
- defensins (antimicrobial peptides)
Oxygen-dependent:
- respiratory burst (toxic metabolites such as superoxide anion, hydrogen peroxide, hydroxyl radical, singlet oxygen)
- reactive nitrogen intermediates (nitric oxide)

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60
Q

How are monocytes and macrophages different?

A

Macrophages are larger, contain lysozyme and phagolysosomes.

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61
Q

What are the types of cytokines?

A

Interleukins
Inteferons
Chemokines
Growth factors (development of immune system)
Cytotoxic (such as Tumour Necrosis Factor)

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62
Q

What are the important interleukins?

A

IL-1: alarm cytokine causing fever
IL-6: acute phase protein
IL-8: chemotactic function for neutrophils
IL-12: directs adaptive immunity and activated NK cells

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63
Q

How can cytokines cause septic shock?

A

Macrophages release massive amounts of TNF-alpha and IL-1. This causes increased vascular permeability and a severe drop in blood pressure.

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64
Q

What is the complement system?

A

A system of glycoproteins and proteins forming a triggered enzyme cascade system.

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65
Q

Where are complements mainly produced?

A

In the liver, and also by monocytes and macrophages.

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66
Q

What are the ways the complement system can be activated?

A
  • Classical pathway (antigen-antibody complexes)
  • Alternate pathway (direct activation by pathogen surface)
  • Lectin pathway (antibody-dependent activation of classical pathway by lectins binding to carbohydrates on pathogens)
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67
Q

What is the Y of complement?

A

How the classical and alternate pathways converge at C3, which leads to the formation of Membrane Attack Complex (MAC).

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68
Q

How is the complement system regulated?

A
  • half-life of components
  • complement is diluted
  • membrane bound and circulating regulatory proteins such as CD59 (which prevents complement related lysis of own cells)
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69
Q

What are the functions of the complement system?

A
  • Lysis
  • Opsonisation
  • Activation of inflammatory response (by fragments)
  • Clearance of immune complexes
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70
Q

What are the functions of mast cells?

A
  • secrete histamine and inflammatory mediators including cytokines
  • recognise, phagocytose and kill bacteria
  • degranulation leads to vasodilation and vascular permeability
71
Q

Give two examples of specialised mast-cells

A

Mucosal mast cells (lungs)

Connective tissue mast cells

72
Q

What type of cell is a natural killer cell?

A

Granulated lymphocyte

73
Q

What are the functions of NK cells?

A

Secrete interferon-gamma
Lyse target cells
Defence against tumours and viral infections

74
Q

How are NK cells inhibited?

A

MHC Class I molecules on self cells bind to Inhibitory receptors.

75
Q

How do NK cells recognise virus-infected cells?

A

These cells express stress-induced receptors on the plasma membrane, which bind to activating receptors on NK cells.

76
Q

What family of molecules do antibodies belong to?

A

Immunoglobulins

77
Q

What are the effector functions of antibodies?

A

Complement activation
Opsonisation
Cell activation via specific antibody binding receptors (Fc receptors)

78
Q

What are the two regions on light and heavy chains on immunoglobulins

A

Variable and Constant regions

79
Q

How many complementarity determining regions are on the Vh and Vl regions.

A

Variable Heavy: 3

Variable Light: 2

80
Q

What is the difference between antibody affinity and avidity?

A

Affinity is the strength of the total non covalent interactions between a single antigen binding site and a single epitope on the antigen.
Avidity if the strength of multiple interactions between an antibody and with multiple binding sites with a complex antigen with multiple epitopes.

81
Q

What is the term used to describe antibodies binding to one or more antigens?

A

Antibody cross-reactivity

82
Q

What part of the antibody have polymorphisms?

A

The constant region

83
Q

What are the names/symbols given to the heavy chains of the different immunoglobulins?

A 
IgG - gamma
IgA - alpha
IgM - mu
IgD - delta
IgE - epsilon
84
Q

What are the different subclasses of IgG and IgA. How do they differ?

A

IgG1 - 4
IgA1 - 2
They differ by having different heavy chains (effector function domains) and different hinge regions. E.g IgG2 has the heavy chain gamma2
They also have different lengths and disulphide bonds.

85
Q

What is the most abundant antibody?

A

IgG

86
Q

What are the properties of IgG?

A
  • Can cross placenta
  • Easily migrate into blood and extracellular fluids
  • Major activator of classical complement pathway (mainly IgG1 and IgG3)
87
Q

What are the properties of IgA?

A

Occurs as a monomer in the blood and a dimer when secreted. It protects mucosal surfaces from bacteria, viruses and protozoa.

88
Q

How do IgA antibodies pass from the blood to epithelial cells to be secreted into a lumen?

A

1) IgA molecules bind to a Poly-Ig receptor allowing the antibody to be taken in by endocytosis.
2) An enzyme in the vesicle cleaves the Poly-Ig receptor from the membrane, leaving it bound to the IgA, forming a secretory component

89
Q

What are the properties of IgA?

A

Occurs as a monomer in the blood and a dimer when secreted (joined by J chain). It protects mucosal surfaces from bacteria, viruses and protozoa.

90
Q

What are the properties of IgM?

A

Forms large pentamers by 5 monomers joined by a J chain.
It is confined to the blood because of its size
It is the first Ig to be synthesised, but tends to have low affinity, but high avidity.
It is effective at agglutination and activating complement

91
Q

What are the properties of IgD?

A

Mainly present in the cell surface of developing B cells. Not expressed as a response to a pathogen.

92
Q

What are the properties of IgE?

A

Produced in respsonse to parasituc infections and allergic disease. Binds to high affinity receptors on mast cells and basophils leading to degranulation.

93
Q

What immunoglobulin(s):

  • Opsonise
  • Activate complement
  • Neutralise toxins
  • Trigger mast cell degranulation?
A
  • IgG
  • IgG, IgM
  • IgG (mainly)
  • IgE
94
Q

What immunoglobulin(s):

  • Neutraluse viruses
  • Agglutinate
  • Neutralise at body surfaces
  • Activate NK cells?
A
  • IgG (mainly)
  • IgM, IgG
  • IgA
  • IgG (mainly)
95
Q

What immunoglobulin(s):

  • Neutraluse viruses
  • Agglutinate
  • Neutralise at body surfaces
  • Activate NK cells?
A
  • IgG (mainly)
  • IgM, IgG
  • IgA
  • IgG (mainly)
96
Q

What immunoglobulin(s):

  • Neutraluse viruses
  • Agglutinate
  • Neutralise at body surfaces
  • Activate NK cells?
A
  • IgG (mainly)
  • IgM, IgG
  • IgA
  • IgG (mainly)
97
Q

What are the two types of adaptive immune responses?

A

Humoral and Cell-mediated

98
Q

Where are B-lymphocytes derived from?

A

Haematopoietic stem cells in the bone marrow

99
Q

What is clonal selection?

A

The process whereby naive lymphocytes are activated and proliferate

100
Q

What is the B-cell receptor?

A

An antibody (mIg - monomeric Ig) associated to a couple of membrane proteins (disufate dunked heterodimers Ig(alpha) and Ig(beta))

101
Q

How does binding of an antigen to a BCR cause an intracellular signal?

A

Binding of antibody to mIg causes a conformational change (BCR clustering) allowing Ig(alpha)/(beta) to signal using their cytoplasmic tail domains.

102
Q

How big is our antibody repertoire?

A

10^10

103
Q

How is antigen diversity generated?

A

immunoglobulin gene rearrangement

104
Q

Whe

A

d

105
Q

What is the B-cell receptor?

A 
An antibody (mIg - monomeric Ig) made of a heavy chain and either kappa or lambda light chains.
Accessory membrane proteins - disulphate dunked heterodimers Ig(alpha) and Ig(beta)
106
Q

How many multigene families exist to code for the BCR mIg?

A

3 - heavy chain, kappa light chain and lambda light chain.

107
Q

What gene segments make up an immunoglobulin light chain?

A

Variable (V), Joining (J) and Constant (C) segments.

108
Q

How many possible gene segments exist for kappa and lambda light chains?

A

Kappa: 40 V segments, 5 J segments and 1 C segment
Lambda: 30 V segments, 4 J segments and 1 C segment

109
Q

How does immunoglobulin gene rearrangement occur?

A

A single V, J and sometimes D segment is chosen at random, and joined together by VD(J) recombinase enzyme complex, containing Rag1 and Rag2 proteins. Unused DNA is looped out and removed. This is then used to create a primary gene transcript.

110
Q

How many possible gene segments exist for kappa and lambda light chains?

A

Kappa: 40 V segments, 5 J segments and 1 C segment
Lambda: 30 V segments, 4 J segments and 1 C segment

111
Q

How does immunoglobulin gene rearrangement occur?

A

A single V, J and sometimes D segment is chosen at random, and joined together by VD(J) recombinase enzyme complex, containing Rag1 and Rag2 proteins. Unused DNA is looped out and removed. This is then used to create a primary gene transcript.
mRNA splicing removes the excess RNA either side of the VDJ genes, producing mature mRNA.

112
Q

How many possible gene segments exist for immunoglobulin heavy chains?

A

65 V segments, 27 D segments and 6 J segments

113
Q

How many possible gene segments exist for immunoglobulin heavy chains?

A

65 V segments, 27 D segments and 6 J segments + multiple C segments determining what type of immunoglobulin it will be.

114
Q

What are the three possible ‘career decisions’ a B-lymphocyte has to make after encountering an antigen?

A

1) Become a plasma cell
2) Become a memory cell
3) Undergo affinity maturation to improve B-cell response

115
Q

Briefly describe how B-cells can be activated

A

Antigen binding to BCR, plus accessory signal from microbial constituents or Thelper cells.

116
Q

How does T-cell independent B-cell activation occur?

A
  • Binding to repetitive antigen (such as bacterial carbohydrate) causing BCR clustering, plus receiving a secondary signal activation by PAMPs binding to Toll-like receptors.
117
Q

How does T-cell independent B-cell activation occur?

A
  • Binding to repetitive antigen (such as bacterial carbohydrate) causing BCR clustering, plus receiving a secondary signal activation by PAMPs binding to Toll-like receptors.
118
Q

How does T-cell dependent B-cell activation occur?

A

An activated T helper cell binds to a B-cell (with bound antigen), providing a co-stimulator response.

119
Q

How does the nature of B-cell activation determine the type of Ig produced?

A 
T-cell independent activation can only lead to the production of IgM.
After T-cell dependent activation, T cell cytokine secretion will determine the type of Ig produced by class switch recombination.
120
Q

How does the nature of B-cell activation determine the type of Ig produced?

A 
T-cell independent activation can only lead to the production of IgM.
After T-cell dependent activation, T cell cytokine secretion will determine the type of Ig produced by class switch recombination.
121
Q

How does the adaptive humoral response change after the primary response?

A

Antibodies are produced faster, and in greater quantities. Antibody affinity is also increased due to somatic hypermutation.
Fewer IgM antibodies are produced, and a lot more IgG are produced.

122
Q

What is somatic hypermutation occur?

A

Essentially natural selection for B-cells. After infection the number of antigens available are significantly reduced. B-cells that bind better to these antigens are more likely to survive than those that don’t.

123
Q

What is somatic hypermutation occur?

A

Essentially natural selection for B-cells. After infection the number of antigens available are significantly reduced. B-cells that bind better to these antigens are more likely to survive than those that don’t.

124
Q

What receptors are found on T-cells?

A

All T-cells have CD3. There are two type of TCR: 90% are (alpha)(beta), 10% are (gamma)(delta).
2/3 of (alpha)(beta) are CD4, 1/3 are CD8

125
Q

What is somatic hypermutation occur?

A

Essentially natural selection for B-cells. After infection the number of antigens available are significantly reduced. B-cells that bind better to these antigens are more likely to survive than those that don’t.

126
Q

How do T-lymphocytes ‘see’ foreign antigen?

A

Via a T-cell receptor binding to an antigen fragment presented by MHC molecules.

127
Q

How is the TCR related to an antibody?

A

It resembles a Fab region.

128
Q

What are the two main types of T-cells?

A

CD8+ cytotoxic (T-killer) and CD4+ T-helper

129
Q

How does TCR binding translate to an intercellular signal?

A

CD3 polypeptides cluster after activation of TCR, causing tyrosine kinases to start a signalling cascade. The motif on the CD3 cytoplasmic tail is called ITAM (Immuno-receptor Tyrosine-based Activation Motif)

130
Q

What are the two main types of T-cells?

A

CD8+ cytotoxic (T-killer) and CD4+ T-helper

131
Q

Outline T-cell development

A

Progenitor cells leave the bone marrow to the thymus where they become thymocytes. They begin their maturation process by migrating towards the medulla.

132
Q

What is the function of the CD8 or CD4 co-receptor?

A

They bind to MHC, increasing the avidity of T-cell target cell interaction.

133
Q

What are the different regions of MHC?

A

Peptide binding region, immunoglobulin like region, transmembrane region and cytoplasmic region in descending order.

134
Q

Describe TCR development

A

Precursors in the cortex are CD4- and CD8- and do not have a TCR.
The alpha unit is similar to the light chain, the beta unit is similar to the heavy chain.
VDJ rearrangement of beta chain occurs first. The beta unit is paired with an alpha surrogate subunit.
If this pairing is successful, the alpha unit is rearranged forming a functioning TCR.
TCRs that do not bind to MHC, and those that bind strongly die by apoptosis. Only TCRs that bind weakly survive.

135
Q

Describe the structure of the MHC Class II molecule

A

Two chains (alpha and beta) of equal size. Both chains have transmembrane and cytoplasmic regions.

136
Q

Describe the structure of the MHC Class I molecule

A

Heavy alpha chain with transmembrane and cytoplasmic region, non-covalently associated with beta2 micro-globulin which just covers the immunoglobulin like region.

137
Q

Describe the structure of the MHC Class II molecule

A

Two chains (alpha and beta) of equal size. Both chains have transmembrane and cytoplasmic regions.

138
Q

What is the difference between the capacity of the MHC Class I and II molecules?

A

MHC Class I can accommodate peptides of 9-10 amino acids

MHC Class II can accommodate peptides of >13 amino acids

139
Q

What is the nature of MHC genes?

A
  • highly polymorphic

- co-dominant

140
Q

What cells display respective MHC Class molecules?

A

MHC Class I: All cells

MCH Class II: Profesional antigen-presenting

141
Q

How are antigens processed?

A 
Endogenous antigens (such as viral proteins) are associated with chaperones and bind to heavy chains of MHC Class I molecules in the ER
Exogenous antigens (such as those captured by phagocytosis) are processed in the endosome. MHC containing vesicles fuse with the endosome
142
Q

Why may a humoural response be insufficient?

A
  • Can’t affect intracellular pathogens

- Some organisms evolve rapidly to escape antibody recognition e.g influenza

143
Q

How does cell mediated immunity protect us?

A

T-cells produce cytokines to activate macrophages to kill ingested microbes or activate inflammatory pathways
CD8+ T-cells kill infected cells, preventing further spread of pathogen

144
Q

How do dendritic cells act as antigen presenting cells?

A

They sample antigens from the environment and move into the lymph nodes to present antigen on MHC Class II molecules.

145
Q

How are T cells activated?

A

Binding of TCR with antigen on MHC Class II molecule, with co-stimulation by cytokines.

146
Q

How are dendritic cells activated?

A

Through PAMPs or DAMPs

147
Q

What are the functions of CD8+ and CD4+ cells?

A 
CD8: 
- cell mediated toxicity
- scans for non-self by looking for an MHC Class I molecule
CD4: 
- macrophage activation
- delayed type hypersensitivity
- B-cell activation
- regulation
148
Q

How do CD8+ cells cause cell mediated cytotoxicity?

A

CD8+ cells that recognise MHC Class I peptide complexes polarise the cell causing the cytotoxic vesicles to face the infected cell. The vesicles are released, inducing apoptosis.
Alternatively, the binding of Fas ligand on the T-cell membrane to the Fas protein causes the same cascade.

149
Q

What proteins do cytotoxic vesicles contain?

A
  • Perforin (form pores in cell membrane allowing other proteins in)
  • Granzymes (serine proteases activate apoptosis)
  • Granulysin (induces apoptosis)
150
Q

How do T helper cells cause macrophage activation?

A

Activated by membrane-bound signals delivered by activated T cells, or by the release of interferon-gamma.

151
Q

What does a macrophage do when activated?

A

Kill phagocytosed bacteria

Secrete increased levels of inflammatory molecules and cytokines to recruit more cells

152
Q

How can a T helper cell activate a B lymphocyte?

A
  • membrane bound BCR recognises antigen
  • antigen is presented in MHC Class II molecules
  • complex recognised by matched CD4+ T-helper cell
  • B-cell becomes activated
153
Q

What are the notable subsets of T helper cells?

A

T helper 1 - produce interferon gamma
T helper 2 - are pro-allergic and boost anti-multicellular organism response
Folicilar T cells - help B cell activation
T helper 17 - secrete IL-17 in autoimmune diseases
T reg - regulate activation ot effector functions of other T cells

154
Q

What are the properties of memory T cells?

A

Express CD45RA
Memory response is stronger and quicker
Effector memory T cells are located at site of infection and immediately assume effector function after infection
Central memory T cells are located in secondary lymphoid tissue and differentiate into effector memory T cells

155
Q

What are the three failures of lymphocyte regulation?

A

1) Autoimmunity
3) Allergy
4) Hypercytokinemia and Sepsis

156
Q

Why is lymphocyte regulation important?

A
  • avoid excessive activation and tissue damage

- prevent inappropriate reactions against self-antigens

157
Q

Define autoimmunity

A

Immune response against self antigen (failure of tolerance)

158
Q

What determines autoimmunity susceptibility?

A

Determined by genes and environmental triggers.

159
Q

Define allergy

A

A harmful response to non-infectious antigens that causes damage and disease

160
Q

What cells play a role in allergy

A

Mast cells cause acute anaphylactic shock

T cells cause delayed-type hypersensitivity

161
Q

What causes hypercytokinemia (Cytokine storm)?

A

Too much immune response caused by positive feedback loop triggered by pathogens entering the wrong compartment or regulation failure.

162
Q

What are the two principles of controlling immune response

A
  • Response giant pathogens decline as infection is eliminated. This is though apoptosis of lymphocytes that lose survival signals.
  • Active control mechanisms that limit responses to persistent antigens
163
Q

What is immunological tolerance?

A

Specific unresponsiveness to an antigen.

164
Q

How is immunological tolerance mediated?

A

Central tolerance (destroying self-reactive T or B cells before they enter circulation) and peripheral tolerance (destroying or controlling self-reacting T or B cells)

165
Q

How is central tolerance achieved?

A

Immature B cells in bone marrow that encounter antigens cross linking their IgM are triggered to undergo apoptosis.
T-cells that bind too strongly to MHC molecules are signalled to undergo apoptosis.

166
Q

How can the thymus express genes of all tissues?

A

Through a specialised transcription factor - AIRE.

167
Q

What do AIRE mutations result in?

A

multi-organ autoimmunity

168
Q

How is peripheral tolerance achieved?

A

Anergy:
- Naive T cells that see its MHC/peptide ligand without co-stimulation become anergic (unresponsive)

Ignorance:
- Immunologically privileged sites do not have
APC
- Antigen may be in too low a concentration to reach threshold for TCR triggering

Antigen-induced Cell Death:

  • Activation through TCR can result in apoptosis depending on the nature of the initial T cell activation
  • Peripheral T cells can be triggered to die by APC expressing Fas ligand

Regulation:
- T regulatory cells produce IL-10 turning off activation.

169
Q

What is the pathophysiology of IPEX?

A

A mutation of the FoxP3 transcription factor of T regulatory cells. This causes Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked syndrome.

170
Q

What are the different types of T regulatory cells?

A
  • Natural Treg (nTreg) developed after recognition of self antigen during T-cell maturation.
  • Inducible Treg (iTreg) develop from mature CD4+ T cells. These may be generated in all immune responses to prevent excessive collateral damage.
171
Q

What are three possible results after an immune response?

A
  • Resolution (no tissue damage; phagocytosis of debris by macrophages)
  • Repair (healing with scar tissue by fibroblasts)
  • Chronic inflammation
172
Q

What are the general surface defences?

A 
Mechanical:
- tight junctions
- fatty secretions waterproofing skin
- social conditioning
Chemical:
- low pH
- fatty acids in skin
- enzymes such as lysozyme
Microbiological:
- Normal flora complete for nutrients/space
- Production of antibacterial substances
173
Q

What are the mucosal surface defences?

A
  • coughing
  • mucus
  • sneezing
  • cilia
  • rapid cell turnover
174
Q

What are the differences between polyclonal antibodies, monoclonal antibodies and myeloma proteins

A

Polyclonal antibodies=A heterogenous mixture of antibodies are produced in response to an antigen.
Monoclonal antibodies=Homogenous, derived from a single B clone.
Myeloma proteins=cancerous plasma cells that divide permanently without antigenic stimulation and secretes antibodies that are indistinguishable from normal antibody.

Year 1 MCD (8 decks)

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