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Immunology > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

1
Q

What cells are involved in adaptive immunity?

A

-B Cells
-T Cells

-Effector T Cells - kill infected cells or help B Cells produce antibodies
-Effector B Cells - produce antibodies against pathogen

-Memory T Cells
-Memory B Cells
—> both mount immune response against previously recognised antigen

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2
Q

Where do the 3 main types of lymphocyte originate from?

A

Common lymphoid precursor (CLP)

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3
Q

What are the 3 main types of lymphocytes originating from CLP?

A

-Natural Killer (NK) Cells
-T Cells
-B Cells

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4
Q

Which lymphocytes are involved in adaptive immune response?

A

-T Cells
-B Cells

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5
Q

What is the generic role of T & B Cells?

A

-Recognise specific antigen - be activated
-Proliferate and differentiate = mediate effector function
-Provide immunological memory

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6
Q

What are antigens?

A

Parts of pathogens (often proteins or parts of proteins) to which T and B cells respond

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7
Q

What part of T & B cells respond to antigens?

A

Antigen rec (highly specific)

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8
Q

What is the structure of a T cell (antigen) rec - TCR?

A

-Either heterodimer or homodimer
-2 chains = alpha & beta - joined by disulfide linkage
-Constant region
-When antigen binds the 2 chains join = activates response

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9
Q

What is the structure of B cell (antigen) rec - BCR?

A

-Antibody structure but bound to memb by transmemb prots = anchors

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10
Q

What is the difference between BCR & antibody?

A

-BCR = anchored to memb of B cells
-Antibody = free

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11
Q

Structure of an antibody?

A

-2 heavy chains
-2 light chains
-Chains joined by disulfide bonds
-Constant regions
-Variable regions

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12
Q

Another term for antibody?

A

Immunoglobulin

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13
Q

What makes a TCR or BCR so specific?

A

-The specific structure of variable region
-Are MANY types of TCR & BCR

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14
Q

Stages involved in an antigen binding to TCR or BCR?

A

-Recognition of peptides (antigens) =
-Activation =
-Proliferation =
-Differentiation (into specific cells)

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15
Q

Roles of T Cells?

A

-Cytotoxicity (cell killing)
-Help of other immune cells
-Regulation (turn off immunity)

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16
Q

Role of B cells?

A

-Produce antibodies =
Neutralisation
Opsonisation
Activate complement pathway

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17
Q

Why is there a faster immune response on secondary infection (by same pathogen)?

A

-Memory B & T cells produced = last long time - ready to respond (& are more effective)

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18
Q

What are the primary lymphoid organs?

A

Bone marrow and thymus

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19
Q

Role of primary lymphoid organs?

A

Where lymphocytes develop & mature from bone marrow derived stem cells

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20
Q

What are 3 secondary lymphoid organs?

A

-LNs
-Spleen
-Mucosa Associated Lymphoid Tissue (MALT)

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21
Q

Role of secondary lymphoid organs?

A

Where coordinate adaptive immune responses

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22
Q

Where do T cells originate & mature?

A

Originate = bone marrow
Mature = thymus

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23
Q

What do TCRs recognise?

A

Peptides

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24
Q

How do TCRs show diversity?

A

Via a genetic mechanism:
-Recombination of segments at alpha & beta locus
-Random segments chosen to make gene - done by large protein complex
-@ alpha locus = V alpha, J alpha, C alpha segments
-@ beta locus = V beta, C beta, J beta, D beta segments
–> GET PAIRING OF RANDOM SEGMENTS TO FORM GENE
-Also get random P & N nucleotides introduced at segment junctions

TCR diversity is generated by the random & imprecise rearrangements of the V & J segments of the TCR alpha (TCRA) & V, D, & J segments of the TCR beta (TCRB) genes in thymus
Thymic production of T cells = sole mechanism to generate TCR diversity

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25
Q

Why are some TCRs without use?

A

Will not bind to peptides - won’t ‘see’ peptides on MHCs of specialised cells

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26
Q

Why are some TCRs dangerous?

A

Bind to self-peptides VERY strongly - so T cells w/ these TCRs will die in development (in thymus)

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27
Q

What is an epitope?

A

Part of an antigen/peptide put in MHC to put on memb of APCs

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28
Q

What type of T cell is a CD8+?

A

Cytotoxic T cell - has CD8 co-receptors (along w/ their TCRs)

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29
Q

What type of MHC (w/ peptide bound) do cytotoxic T cells recognise?

A

MHC I (one)

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30
Q

Role of MHC I?

A

Presents antigens/peptides on ALL NUCLEATED body cells (so all body cells can be APCs)

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31
Q

Function of CD8+ cytotoxic T cells?

A

Kill virus-infected cells directly

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32
Q

What type of T cell is a CD4+?

A

Helper T cell - has CD4 co-receptors (along w/ their TCRs)

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33
Q

What type of MHC (w/ peptide bound) do helper T cells recognise?

A

MHC II (two)

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34
Q

Role of MHC II?

A

Presents antigens only on ‘professional’ APCs

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35
Q

Function of CD4+ helper T cells?

A

-Produce cytokines - activate other immune cells
-Express surface molecules to affect other cell types

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36
Q

Which way around do CD8+ and cytotoxic T cells form?

A

CD8+ T cells –> form cytotoxic T cells

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37
Q

Which way around do CD4+ and helper T cells form?

A

CD4+ T cells –> form helper T cells

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38
Q

What are effector T cells?

A

-Cytotoxic T cells
-Helper T cells
–> form from CD?+

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39
Q

Summarise CD? T cell effector type, MHC type and function.

A
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40
Q

How do CD? and MHC and TCR relate?

A

Peptide in TCR on MHC - interacts w/ CD (co-receptor of CD4+ or CD8+ T cell)?

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41
Q

What is an example of a professional APC?

A

-Dendritic cells - initiates adaptive immunity (links innate to adaptive)

-Macrophages
-B cells

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42
Q

What type of MHC do dendritic cells present antigens on, & what does this mean?

A

BOTH –> MHC I & MHC II
–> so can activate CD8 (MHC I) & CD4 (MHC II) T cells

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43
Q

When & how do dendritic cells mature?

A

-When PAMPs (things on pathogens) or DAMPs (things from damaged cells) stimulate
–> causes production of molecules to activate naïve T cells
–> move to secondary lymphoid tissue

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44
Q

What cells express MHC I?

A

ALL nucleated cells (ones w/ nuclei - so NOT RBCs)
–> so nuc cells = can activate CD8 T cells

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45
Q

What genes in MHC I code for the peptide binding groove - which antigens can bind?

A

MHC class I molecules are encoded by 3 different loci, A, HLA-B, HLA-C = x3 types of MHC proteins
—> So HLA-A, HLA-B, HLA-C antigens bind to 1/3 of the MHC I protein peptide binding grooves

(3 genes - 6 alleles)

—> HLA = gene complex on short p arm of chromosome 6

46
Q

What genes in MHC II code for the peptide binding groove - & what antigens bind to these?

A

MHC class II molecules are encoded by 3 different loci, HLA-DR, HLA-DQ, HLA-DP = x3 types of MHC proteins
—> So HLA-DR, HLA-DQ, HLA-DP antigens bind to 1/3 of the MHC II protein peptide binding grooves

(3 genes - 6 alleles)

—> HLA = gene complex on short p arm of chromosome 6

47
Q

What do other MHC genes code for?

A

Proteins to process antigen

48
Q

Where does peptide from pathogen bind to in MHC I & II?

A

Antigen binding groove of the Human Leukocyte Antigen (HLA)

49
Q

How are the peptides that are presented, produced in APCs?

A

Large protein antigens = digested = smaller (these = different epitopes of antigen)

50
Q

Features of MHC I?

A

-Expressed by nucleated cells
-Binding groove holds short peptides (8-10 AAs)

51
Q

Features of MHC II?

A

-Expressed by professional APCs
-Binding groove holds longer peptides (13-17 AAs)

52
Q

Features of MHC genes?

A

-Polygenic = several MHC genes
-Polymorphic = variation in pop

53
Q

How do MHC I present peptides?

A

-Virus infects body cell
-Proteosome chops virus up
-Viral particles synthesised in ER
-Antigens put onto MHC I (IN ER)
-MHC I w/ antigen presented on memb = APC
-TCR of CD8+ helper T cell binds = activated

54
Q

How do MHC II present peptides?

A

-APC phagocytoses pathogen
-Phagolysosomes break down pathogen
-Antigens put onto MHC II (in phagolysosome)
-MHC II w/ antigen presented on memb = APC
-TCR of CD4+ T = activated

55
Q

What about naive T cells - how are they initially activated?

A

3 signals needed
1 = Antigen binds to TCR
2 = Costimulation
3 = Cytokines
–> all provided by dendritic cell

56
Q

What is involved in signal 1 - antigen binding to TLR - in activating naive T cells?

A

Peptide MHC complex (on dendritic cell) binds to TCR
–> immune synapse formed if TCR recognises antigen

57
Q

What is involved in signal 2 - costimulation - in activating naive T cell?

A

-TLR signalling in dendritic cell = upregulate costimulatory molecules - B7
-B7 interacts with CD28 on T cell
= costimulation

58
Q

What is involved in signal 3 - cytokines - in activating naive T cells?

A

-APCs produce cytokines
-Cytokines cause T cell differentiation into specific effector cell
–> cytotoxic OR helper

59
Q

Summarise naive T cell activation.

A
60
Q

Which T cells do not need the 3 stages of activation - can just exert their function?

A

Effector T cells:
-Cytotoxic
-Helper
—> meaning T cells which are NOT naïve (previously been activated by DC)

61
Q

What are the 5 types of effector CD4 T helper cell?

A
62
Q

Define polarising cytokine.

A

Cytokine which activates

63
Q

What is the polarising cytokine (from APC) for TH1?

A

IL-12

64
Q

What is the polarising cytokine (from APC) for TH2?

A

IL-4

65
Q

What is the polarising cytokine (from APC) for TH17?

A

IL-6
IL-21

66
Q

What is the polarising cytokine (from APC) for TFH?

A

IL-6
TGFβ
IL-23

67
Q

What is the polarising cytokine (from APC) for Treg?

A

TGFβ

68
Q

What is the TF for TH1 - to produce cytokines?

A

T-bet

69
Q

What is the TF for TH2 - to produce cytokines?

A

GATA3

70
Q

What is the TF for TH17 - to produce cytokines?

A

RORγT

71
Q

What is the TF for TFH - to produce cytokines?

A

Bc16

72
Q

What is the TF for Treg - to produce cytokines?

A

FoxP3

73
Q

What cytokines are produced by TH1?

A

IFNγ

74
Q

What cytokines are produced by TH2?

A

IL-4
IL-5
IL-13

75
Q

What cytokines are produced by TH17?

A

IL-21
(& IL-4 or IFNγ)

76
Q

What cytokines are produced by Treg?

A

IL-10
TGFβ

77
Q

What is the primary function of TH1?

A

Activate macrophages

78
Q

What is the primary function of TH2?

A

-Activate eosinophils & mast cells
-Alternative macrophage activation

79
Q

What is the primary function of TH17?

A

Enhance neutrophil response

80
Q

What is the primary function of TFH?

A

Activate & mature B cells

81
Q

What is the primary function of Treg?

A

Suppress other effector T cells

82
Q

Summarise T helper cell cytokine signals.

A
83
Q

What do CD8+ cytotoxic effector T cells do?

A

Kill virus infected cells in tissue –> once TCR has recognised (bound) to MHC I/peptide complex

84
Q

How do cytotoxic T cells kill virus infected cells - 2 ways?

A

-Perforin/granzyme
-Fas : FasL ligand interaction

85
Q

How does perforin/granzyme kill virus infected cells?

A

-CD8+ T cells exocytoses lytic granules (perforin + granzymes) @ immune synapse (between TCR & MHC/peptide)
-Perforins (part of granule) = forms channel in target cell
= granzymes enter cell
-Cascade of reactions = DNA cleavage - so cell death

86
Q

How does Fas : FasL ligand interaction kill virus infected cells?

A

-FasL = expressed by cytotoxic T cell
-Fas = expressed by target cells
-Fas : FasL interact
= activates FADD –> then pro-caspase 8 activated (in target cell)
-Causes apoptosis of target cell
-Caspases (cysteine proteases that cleave aspartic acid) = activated in apoptosis
= ordered cell destruction

87
Q

How can CD4 helper T cells help activate CD8 cytotoxic T cells?

A

-Activated CD4 helper T cell expresses CD40L (on surface) & IL-2 = stimulated by APC
-IL-2 = cytokine to help activate cytotoxic T cell
-B7 involved too

88
Q

What is cross-presentation?

A

How antigen taken up by phagocytosis (so is currently on MHC II) gets loaded onto MHC I (important for anti-tumour & anti-viral immunity - as only MHC I can activate CD8+ cytotoxic T cells for this)

—> possible because professional APCs have MHC I & II

89
Q

Where do B cells develop & mature?

A

Bone marrow - have BCR when leave (recombined antigen rec)

90
Q

What are the effector cells of B cells?

A

-Plasma cells
-Memory B cells

91
Q

What are the 2 types of antibody?

A

-BCR antibodies - anchored into memb of B cell
-Soluble/free antibodies - produced by plasma B cells

92
Q

How are the different types (diversity) of BCRs formed?

A

-Heavy chain locus
-Light chain loci = Lamba (λ) locus & kappa (κ) locus
–> select, recombine gene segments = functional gene
*** Rearrangement at heavy & light Ig chain loci

-Random nucleotides added or removed at segment junctions

93
Q

How do BCRs work?

A

Directly bind to antigens - even if still bound to pathogen

94
Q

What are T dependent B cell responses?

A

-B cell presents antigen on BCR
-T cell (already activated by APC - dendritic cell) provides CD40L & cytokines to B cell
= activates B cell

95
Q

Signal 1 in B cell activation?

A

= BCR signalling & uptake
-BCR recognises antigens on pathogens
-B cell takes up antigen = processed, broken down (phagolysosome) = peptides
-Peptides put onto MHC I - onto memb
-B cell = APC
-CD4+ T helper TFH cells = TCR binds to antigen***

96
Q

Signal 2 in B cell activation?

A

= co-stimulation
-CD40 of B cell interacts w/ CD40L of T cell

97
Q

Signal 3 in B cell activation?

A

= cytokines
-Produced by T cell = instructs B cell to produce certain antibodies

98
Q

Summarise B cell activation.

A
99
Q

What does productive CD4+ helper T cell & B cell interaction cause?

A

Proliferation & differentiation into:
-Plasma cells = antibody
-Memory cells

100
Q

What do cytokines (released by T cell) do to B cells?*???

A

Causes class switching = so antibodies of various classes - isotypes form
IgG
IgE
IgD
IgM
IgA

101
Q

What is different about different classes of antibodies?

A

Different heavy chain constant region - linked to particular function

102
Q

Purpose of class switching of B cells?

A

Make different types or isotypes of antibody, suited to fight the infection/protect host in future

103
Q

Roles of the 5 classes of antibodies?

A
104
Q

Summarise what types of cytokines (produced by T cell) induce & inhibit different antibody classes.

A
105
Q

Role of IgA & IgG?

A

= Neutralisation
-Bind to bacterial toxins & virus particles - stops these binding to recs (no tissue damage)

106
Q

Role of IgG?

A

= Opsonisation
-Bind to pathogens
-Phagocytes recognise these bound antibodies (by Fc rec)
= phagocytosis & killing

107
Q

Role of IgM & IgG?

A

= Complement activation
-Bind to pathogens - activates complement pathway (via C1q)
-So memb attack complex forms = kills pathogen

108
Q

Role of IgG?

A

= Natural killer cell sensitisation
-Bind to virus infected host cells
-NK cells recognise antibody bound (via Fc rec)
-NK = kills cells

109
Q

Role of mast cells in terms of antibodies?

A

-Have Fc recs
-Recognise IgE
-Antibodies cross-link by antigens
= mast cell degranulation –> histamine released

110
Q

Role of eosinophils in terms of antibodies?

A

-Recognise IgE bound to parasites & release granules to kill the parasite

111
Q

Role of basophils in terms of antibodies?

A

-Recognise IgD = activates anti-microbial & pro-inflammatory mechanisms

112
Q

Where do peptides/antigens bind in relation to MHC & what genes encode this?

A

Peptide epitopes are bound in the peptide-binding groove of the Human Leukocyte Antigens (HLA) encoded by Major Histocompatibility Complex (MHC) genes

Immunology (6 decks)

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