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MIMM 214 > Midterm > Flashcards

Midterm Flashcards

1
Q

Immunization Types

A

Active-Natural: Infection
Active-Induced: Vaccination
Passive-Natural: mother’s breast milk & mother to fetus
Passive-Induced: antiserum

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2
Q

Primary (central) Lymphoid Organs

A

Bone Marrow

Thymus (above heart)

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3
Q

Secondary (peripheral) Lymphoid Organs

A

Lymph nodes
Spleen
Malt/Payer’s Patch (in gut)

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4
Q

Leukocyte

A

immune system cell (white blood cell)

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5
Q

Lymphoid lineage cells

A 
B cells
T cells
NK cells
innate lymphoid cells
some dendritic cells
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6
Q

Myeloid lineage cells

A

macrophages
neutrophils (and other granulocytes)
monocytes
some dendritic cells

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7
Q

Leukocyte lineages

A

Lymphoid, Myeloid

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8
Q

Lymphocytes & properties

A

B cells and T cells (adaptive immunity)

Arise from bone marrow

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9
Q

Lymphocyte receptors

A 
BCR:
 - secreted or membrane bound
 - bounds antigen in natural form
TCR 
 - membrane bound
 - binds MHC with small piece of antigen on it
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10
Q

MHC

A

Major Histocompatibility Complex

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11
Q

Clonal Deletion

A

lymphocytes binding self-antigens are eliminated

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12
Q

Naive lymphocyte

A

mature lymphocyte not yet activated by an antigen

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13
Q

Innate immunity barriers/obstacles

A

Barriers: skin, epithelium (gut, respiratory tract)
Obstacles: saliva, hair, mucus, tears

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14
Q

Lyzozyme

A

digests peptidoglycan

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15
Q

Defensins

A

disrupts cell membrane by forming pores

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16
Q

Phagocytosing cells

A

macrophages
neutraphils & other granulocytes
immature dendritic cells

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17
Q

Phagocytosis steps

A
  • receptors bind pathogen
  • phagosome formed by invagination
  • phagolysosome formed by fusion with lysosome
  • digestion
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18
Q

Phagocytosis digestion methods

A

acidification
ROSs
enzymes
antimicrobial peptides

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19
Q

microglia

A
  • phagocyte working in the central nervous system

- cleans up myelin debris from neurons

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20
Q

multiple sclerosis

A

demyelination of neurons

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21
Q

Leukocyte migration process

A

cytokines/chemokines released at site of infection

  • > blood vessels dilate and adhesion molecules expressed
  • > leukocytes extravasate
  • > bloot clotting, pain, redness, edema
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22
Q

Extravasation process

A

chemokines bind to endothelial cell

  • > leukocytes roll into and bind tightly to endothelium
  • > cells change shape
  • > induced diapedesis
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23
Q

diapedesis

A

Passage of cells through wall of capillaries, inducing inflammation

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24
Q

Monocyte

A

circulating leukocyte

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25
Q

Neutrophil

A
  • innate immune system phagocyte
  • circulating - must be recruited
  • pus is product of dead/dying neutrophils
  • produces NETs (neutrophil extracellular traps) matrix that traps microorganisms
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26
Q

Complement molecule properties

A
  • mostly proteases
  • usually named C_ (number), and C_a, C_b… when cleaved
  • mostly produced by liver
  • part of chain reactions that amplify inflammation and clearing of pathogens
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27
Q

Complement mechanisms of action

A

Increase vascular permeability and chemotaxis
Destroy pathogen membranes
Opsonization

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28
Q

Opsonization

A
  • Coating a pathogen to make it more easily ingested by phagocytes (by antibodies and similar molecules)

C3b coats bacteria

  • > binds C3b receptors on phagocyte
  • > cascade leading to phagocytosis
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29
Q

Complement Activation (general)

A

Complement components begin as inactive pro-proteases
Cascade of events leads to proteolotic cleavages
- small piece that has a function
- large piece that acts as protease to another substrate
All pathways converge to C3 convertase cleaving C3 to C3a and C3b
Main pathways:
- lectin pathway
- classical pathway
- alternative pathway

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30
Q

Lectin Pathway

A

Specific PRRs bind directly to pathogen cell membrane

  • > signaling cascade on surface
  • > C3 convertase generated
  • > C3a and C3b produced

PPRs:

  • mannose-binding lectin, ficolins
  • circulating in blood
  • upregulated during infection
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31
Q

Classical Pathway

A

C1q in blood binds either to pathogen cell membrane (direct) or to antibody bound to pathogen membrane (indirect)

  • > signaling cascade on surface
  • > C3 convertase generated
  • > C3a and C3b produced
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32
Q

Alternative Pathway

A

Triggered by existing C3b present due to spontaneous hydrolysis, or production from other pathways

C3b binds other factors

  • > produce a particular unstable C3 convertase
  • > stabilized by Properdin
  • > more C3b produced
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33
Q

Properdin

A

aka Factor P
Produced by neutrophils
Stabilizes the alternative pathway C3 convertase

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34
Q

Complement induced inflammation

A

C3a & C5a increase vascular permeability and chemotaxis
(too much -> anaphylactic shock)
C3a & C5a bind receptors on granulocytes and macrophages
-> stimulate release of proinflammatory cytokines & degranulation

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35
Q

Complement induced pathogen lysis

A

Cascade of events creating MAC (membrane attack complex)

  • > pore on pathogen surface
  • > cell lysis
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36
Q

Innate Lymphoid Cell

A
  • three types (ILC1, ILC2, ILC3)
  • mainly tissue resident (recent studies show otherwise)
  • important in gut mucosa
  • activated by cytokines (IL-25 is well known to)
  • release other cytokines that contribute to pathogen death
  • recent finding shows migration of ILC2 between guts and lungs through lymph vessels
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37
Q

Natural Killer Cells

A
  • kills own infected cells
  • found in tissues and in circulation
  • receptors are germ-line encoded
  • recognize MHC1 & similar proteins

Non-Disease State: inhibitory signals on cell prevent NK activation
Disease State: inhibitory signal not present
-> NK releases toxic granules -> apoptosis
OR
-> receptor-mediated apoptosis

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38
Q

Common Proinflammatory Cytokines

A

TNF-alpha, IL-1beta, IL-6

39
Q

Proinflammatory Cytokine effects

A
  • vascular permeability and chemotaxis
  • have different effects on different tissues/organs
    ex: hypothalamus -> fever, liver -> acute inflammatory response
40
Q

Local infection process

A

local TNF-alpha release

  • > vasodilation & leukocyte migration
  • > clearing of infection
  • > draining of extracellular fluids to lymph nodes
41
Q

Sepsis process

A

systemic TNF-alpha release

  • > system vasodilation
  • > lowering of blood pressure
  • > collapse of blood vessels
  • > intravascular coagulation
  • > organ failure and death
42
Q

TNF-alpha

A

released by macrophages

target of some autoimmune drugs

43
Q

Acute Inflammatory Response

A

Increased production from liver:

  • mannose-binding lectin
  • complement components
  • C-reactive proteins

Positive feedback loop until clearing of infection

44
Q

PRRs

A
  • Recognize PAMPs
  • Activate signaling pathways, typically involving phosphorylation and ubiquination cascades
  • expressed by many cells
45
Q

PRR groups

A 
Toll-like receptors
NOD-like receptors
RIG-like receptors
C-type lectin receptors
ficolins
46
Q

Toll-like Receptors

A

Location:

  • cellular membrane (for bacteria, parasites)
  • endosome membrane (for viruses, bacteria)

Usually have adapter proteins

Activates TFs -> proinflammatory cytokine genes
Common Pathways:
- NF-kB
- IRF
- MAP kinase
47
Q

RIG-like Receptors

A

Location: cytosol
Recognize viral dsDNA

Triggers TFs
Common Pathways:
- NF-kB
- IRF

48
Q

NOD-like Receptors

A

Location: cytosol
Recognize peptidoglycans

Can trigger NF-kB TFs
Can activate caspase-1 (protease)
- cleaves IL-1/IL-18 to activate them, then release

49
Q

PRR Signaling Downstream Effects

A
  • cytokine production (IL-1, IL-6, IFN)
  • B7.1 B7.2
  • migration to secondary lymph organs (for APCs)
50
Q

Type 1 IFN

A

IFN-alpha and IFN-beta

- triggers transcription of genes that inhibit viral replication

51
Q

Cytokine

A

small glycoprotein

52
Q

Cytokine communication mechanisms

A

Autocrine (self)
Paracrine (nearby)
Endocrine (far)

53
Q

Cytokine categories

A 
Interleukins
Interferons (type 1, type 2)
Tumor Necrosis Factor
Hematopoetins or growth factors
Chemokins
54
Q

Lymph Node Migration

A

Activated DCs: enter by afferent lymph vessel
T Cells:
- enter by High Endothelial Venules (HEV)
- leave by efferent lymph vessel

55
Q

Plasmacytoid DC

A
  • stays at infection site
  • produces large amount of type 1 IFN
  • produces many PRRs
56
Q

Unactivated DC Characteristics

A

Highly phagocytic

Many dendrites

57
Q

PAMP Induces what on DC

A
  • receptors that target DC to LT
  • antigen processing genes (MHC)
  • costimulation proteins
58
Q

Activated DC Characteristics

A
  • can no longer phagocytose
  • less dendrites
  • homes into lymphoid tissues
59
Q

Three Activation Signals

A

Activation
Survival
Differentiation

60
Q

T-Cell Migration through Endothelium

A

rolling -> tight binding -> diapedesis -> chemokines

selectins and integrins guide T-Cell to different sites

61
Q

T-Cell classes

A

CD8+ becomes Cytotoxic T Lymphocyte

CD4+ becomes helper T Cell of a particular subtype

62
Q

CD4+ subtypes

A

TH1, TH2, TH17, Treg, Tfh

  • each subtype:
    • activated via different cytokine
    • has distinct cytokine profile
    • regulates distinct activities
63
Q

Immunological synapse

A

tight binding between pMHC and TCR during activation

64
Q

CD3

A
  • flank TCR, helps with binding

- all T Cells express it

65
Q

Zeta chains

A

transmembrane protein part of TCR

66
Q

ITAM Motif

A

part of zeta chains on TCR

get phosphorylated as part of signalling cascade

67
Q

TCR subunits

A

Heterodimer made of alpha and beta chains, or gamma-delta
(90% alpha-beta)
- conneced by disulfide bridge

68
Q

Clonotypic

A

each cell expresses own type of something

69
Q

MHC1

A 
present endogeous peptides (usually)
activates CD8+ T Cells
alpha chain with 3 domains
beta microglobulin domain (non-transmembrane)
binds short 8-10 aa peptides
expressed by all nucleated cells
70
Q

MHC2

A 
present exogenous peptides (usually)
activates CD4+ T cells
alpha chain with 2 domains
beta chain with 2 domains
only expressed by professional APCs
binds peptides of any length
71
Q

MHC Genetic Variation

A

Peptide binding cleft has lots of allelic variation

Rest of MHC is highly conserved

72
Q

Co-Receptors Structures

A

CD4 - single chain, 4 Ig-like domains

CD8 - heterodimer linked by S bridge, alpha and beta Ig like domains

73
Q

TAP

A
  • transmembrane protein on ER
  • deliver peptides from cytosol to ER
  • site of peptide loading on MHC1
74
Q

Calnexin

A

chaperone holding together partially folded MHC1 alpha chain

75
Q

Tapasin

A

chaperone that links MHC1 and TAP

76
Q

Invariant Chain

A
  • binds and blocks peptide binding groove of MHC2
  • directs MHC2 to vesicles (using tail)
  • degrades to CLIP
77
Q

CLIP

A
  • piece of invariant chain

- blocks peptide groove of MHC2

78
Q

HLA-DM

A
  • inside MHC2 vesicle

- binds MHC2 and releases CLIP

79
Q

Cross-Presentation

A

CD4+ T cells license APCs to cross-present

- back and forth cytokine signal

80
Q

Autophagy Ag presention

A

sends endogenous antigen to exogenous pathway

81
Q

MHC Restriction

A

given T-cell can only recognize specific peptide bound to a specific self MHC

82
Q

Allorecognition

A

1-10% of all T cells recognize and react to non-self MHC, regardless of presented peptide

83
Q

MHC Gene

A

human leukocyte antigen (HLA)

codes for MHC

84
Q

MHC1 Genes

A

HLA-A, HLA-B, HLA-C, code for the alpha chain

85
Q

MHC2 Genes

A

HLA-DR, HLA-DQ, HLA-DP, etc. code for alpha and beta chains

86
Q

MHC polymorphism

A

> 100 different alleles

usually amino acid changes in peptide-groove

87
Q

SH2 Domain

A

Adaptor/scaffold structure that bind protein to bring them in proximity/orientation

88
Q

pMHC:TCR Signaling

A

pMHC:TCR

  • > co-receptor binding
  • > recruitment of Lck
  • > Lck phosphorylates ITAMs
  • > ZAP-70 is phosphorylated
  • > ZAP-70 activates four different signaling pathways
  • > transcription of genes necessary for T cell activation
89
Q

Costimulation proteins

A

Ligands on APC:
CD80 (B7.1)
CD86 (B7.2)

Receptors on T Cell: CD28

90
Q

CD28

A

Transmembrane glycoprotein. Homodimer.
Found in close proximity to TCR
Expressed on all naive T cells at resting condition
Binds CD80, CD86 -> triggers phosphorylation of CD28
Required for activation and proliferation

91
Q

Clonal Anergy

A

Signal 1 in absence of Signal 2 results in transcription of anergy genes

Anergetic T cell no longer responsive to stimulation

92
Q

IL-2

A

Cytokine working in autocrine manner

93
Q

IL-2 cascade

A

Signal 1 + Signal 2

-> cascade leading to binding promoter region of IL-2 gene and IL-2Ralpha (or CD25) gene

94
Q

IL-2R subunits

A

alpha, beta, gamma

beta and gamma are expressed at baseline level

MIMM 214 (1 decks)

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