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Biomed year 2 sem 1 > CMB2004- Immune system > Flashcards

CMB2004- Immune system Flashcards

1
Q

Adaptive/ specific immunity

A

induced by exposure to particular infection
highly specific
exhibits memory

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2
Q

specific immunity is mediated by

A

B/T lymphocytes

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3
Q

clonal selection theory

A
  1. removal of self-reactive immature lymphocytes from the repertoire
  2. pool of immature lymphocytes for foreign antigens
  3. proliferation & differentiation of specific lymphocytes -> clone of effector cells
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4
Q

BCR =

A

B cell receptor
- expressed by B lymphocytes

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5
Q

antibodies are secreted when….

A

B cell is activated

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6
Q

TCR =

A

T cell receptor
- expressed by T lymphocytes

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7
Q

TCR will only recognise…(1) bound to…(2)

A
  1. peptide fragments of antigen
  2. MHC expressed by APC
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8
Q

Antibody functions

A
  • help with infection by encapsulated bacteria
  • activate complement system
  • activation of effector cells
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9
Q

antibody structure

A

4 polypeptides each with variable and constant regions
- heavy chain and light chains

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10
Q

Fab region on antibody

A

Fragment antigen binding

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11
Q

Fc region on antibody

A

fragment constant

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12
Q

5 antibody classes/isotopes

A

IgM, D, A, G, E

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13
Q

isotype is determined by…

A

C region heavy chain

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14
Q

Domains =

A

patterns present in many other proteins in the immune system

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15
Q

how many domains does the L chain have

A

2

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16
Q

how many domains does the H chain have

A

4/5

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17
Q

what links L chain and H chain

A

disulphide bridge

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18
Q

Hypervariable regions

A

concentrated region of variability
3 in VH, 3 in VL (HV1-3)

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19
Q

CDR =

A

complementary-determining regions
- determine specificty and affinity of ab for ag

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20
Q

epitope

A

bit of antibody that recognises antigen

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21
Q

antibody and antigen form… interactions

A

non-covalent

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22
Q

MHC class 1 in humans

A

HLA-A, -B, -C

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23
Q

MHC class I expressed on…

A

all nucleated cells

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24
Q

MHC I structure

A
  • heterodimer: alpha chain and beta2 microglobulin
  • a1 and a2 domains fold -> b-sheet -> peptide binding site
  • a3 domain + b2 microglobulin fold -> Ig-like domains
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25
Q

MHC 2 expressed on…

A

APCs + cytokine activated cells

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26
Q

MHC II in humans

A

HLA-DP, HLA-DQ, HLA-DR

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27
Q

MHC II structure

A

heterodimers a and b chaims are both transmembrane
- a2 and b2 domains are Ig-like
- grooves are more open than in class 1, bind longer peptides

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28
Q

H chain and TCRb V region encoded by

A

3 gene segments:
V, D, J

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29
Q

L chain and TCRa encoded by

A

V, J

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30
Q

NHEJ

A

non-homologous end joining region
- genes rearranging during B cell development to form a functional gene

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31
Q

steps of NHEJ

A
  1. DNA breaks between V+J
    -> brings together a V chain and a C chain -> light chain genome
  2. V, D,J segment join together in a single B cell -> V region of the heavy chain
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32
Q

hierarchy of gene rearrangements

A
  • first heavy chain genes: D-J then V-D
  • then light chain genes: kappa then V-J
  • if kappa rearrangement is unsuccessful -> genes rearrange
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33
Q

H chain chromosome

A

14

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34
Q

kappa chain chromosome

A

2

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35
Q

kappa chain chromosome

A

2

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36
Q

delta chain chromosome

A

22

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37
Q

RSS

A

Recombination Signal Sequences
- special sequences flanking the VDJ regions -> guide rearrangement

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38
Q

RSS enzyme complex

A

V(D)J recombinase - recombination activating gene (RAG)

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39
Q

RAG1 and RAG2 genes encode…

A

lymphoid specific components of the V(D)J recombinase
mutations -> immunodeficiency

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40
Q

Allelic exclusion

A

single B cell = only one allele of H and L is expressed
- single B cell expresses kappa or delta, never both
- light chain isotype exclusion
-> individual B cell only produces one specific antibody

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41
Q

antibody combinational diversity

A

different VDJ segments recombine to produce different segments

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42
Q

antibody junctional diversity

A
  • imprecise joining
  • N regions: random nucleotide addition of nucleotides at V-D and D-J junctions by terminal transferase
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43
Q

somatic hypermutation

A
  • mutation frequency in antibody VH gene is higher than normal spontaneous mutation rate
  • occurs in germinal centres as B cells recognise Ag and proliferate/activate
  • involves AID enzyme
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44
Q

AID enzyme

A

Activation-induced deaminase
acts on DNA to convert cytosil to uracil -> recognise by error prone DNA repair pathways -> mutations

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45
Q

constant region of each heavy chain is encoded by…

A

a different C region gene segment

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46
Q

IgM heavy chain gene

A

C upsilon (u)

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47
Q

IgD heavy chain gene

A

C delta

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48
Q

IgG heavy chain gene

A

C gamma (y)

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49
Q

IgA heavy chain gene

A

C alpha (a)

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50
Q

IgE heavy chain gene

A

IgE epsilon

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51
Q

Ig class switching

A

requires further DNA recombination, guided by switch regions
- involves the AID enzyme
pathpgen -> cytokine -> switch

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52
Q

TBR receptor genes

A

encoded by VDJ segment rearrangement

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53
Q

TCR generating diversity

A
  • similar to BCR ( combinational, junctional diversity)
  • NO somatic hypermutation
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54
Q

MHC genes

A

No gene rearrangement
- genes located within MHC (HLA in humans - chromosome 6)
- extremely polymorphic

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55
Q

MHC polymorphism

A

allows binding of a wide range of peptides to T cells -> clear evolutionary advantage
downside: increases risk of immune mediated diseases, makes organ donation complicated and inefficient

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56
Q

how do peptides get to the surface of cells with MHC I molecules

A
  • intracellular antigen processing to peptides in proteasome
  • peptide transport into ER
  • peptide binding by MHC I
  • MHC class I presents peptide at cell surface
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57
Q

TAP

A

component of multi-protein assembly
- peptide loading complex - includes tapasin and calreticulin

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58
Q

Antigen processing and presentation by MHC II molecules

A
  1. Ag endocytosed into IC vesicles
  2. protein cleaved by acid proteases in vesicles -> peptides
  3. vesicles fuse with visicles containing MHC II
  4. peptides bind MHC II
  5. complex is transported in vesicles to cell surface
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59
Q

MHC class 1 accessory molecules

A

TAP and LMP

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60
Q

MHC class 2 accessory molecules

A

HLA-DM

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61
Q

B cells develop from… that express….

A

haemopoietic stem cells
PAX5 transcription factor

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62
Q

stages of B cell development

A
  1. Generation of B cell receptors in bone marrow
  2. negative selection (self-reactive removed)
  3. migration of B cells through blood to lymphoid organs -> B-cell activation by foreign antigen
  4. antibody secretion and memory cells in bone marrow and lymphoid tissue
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63
Q

what happens if a B cell doesn’t encounter an antigen

A

it dies

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64
Q

formation of pre-B cell receptor

A

Early pro-B cell -> Vh, DJh rearrangements occur -> large pre-B cell -> stop heavy chain gene rearrangements -> light chain continues rearranging in small pre-B cells -> immature B cell -> stops light-chain rearrangement -> mature B cell

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65
Q

pre-BCR signal

A
  • Turns off RAG-1 and -2 genes
    -> 5-6 rounds of cell division
    -> surrogate light chain expression stops
    -> RAG genes turned back on
    -> L chain rearrangement starts
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66
Q

immature B cells only express…

A

IgM

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67
Q

immature B cells that bind multivalent self-antigens…

A
  1. clonal deletion -> apoptosis
  2. receptor editing -> further light chain gene rearrangements (give it another chance)
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68
Q

immature B cells that bind soluble self-antigen

A

cell becomes unresponsive (anergic)

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69
Q

T cells develop in the…

A

Thymus

70
Q

steps of T cell development

A
  1. notch signalling -> precursors commit to T-cell lineage, self reactive are removed
  2. T cells activated by foreign antigens, migrate to peripheral lymphoid organs
  3. activated T cells migrate to sites of infection -> proliferate and eliminate
71
Q

once T cell precursors reach thymus they develop into…

A

thymocytes

72
Q

thymocytes

A
  1. rearrange TCR genes (b first) and express TCR
  2. Aquire other markers e.g. CD3, 4, 8
  3. positive and negative selection
73
Q

Thymus

A

bi-lobed organ in ant. mediastinum
cells: lymphoid cells, epithelial cells, macrophages, dendritic

74
Q

T-cell maturation in thymus

A
  • pro-thymocytes enter cortex from bone marrow
  • rearrange TCR, 1st TCRb then pre-TCRa -> pre-TCR
  • cells proliferate then rearrange TCRa genes
  • express TCR together with CD3
  • also express CD4 and CD8 - peripheral T cells express one or the other
75
Q

TCR expression requires…

A

CD3 complex
- CD£ transmits a signal to T cell nucleus after TCR recognition

76
Q

T cells expressing a randomlt rearranged abTCR may:

A
  1. recognise forgeign Ag - immunity
  2. recognise self-Ag - autoimmunity
  3. not be able to recognise self-MHC - useless
    - need to keep 1 and eliminate 2/3
77
Q

T cell positive selection

A
  • occurs when CD4+/CD8+ T cells recognise MHC on cortical epithelial cells in thymus
  • not recognised -> apoptosis
78
Q

T cell negative selection

A

on dendritic cells/macrophages with high affinity
- TCR binding self-peptide -> apoptosis

79
Q

naive T cells

A

blood -> lymph node via HEV -> move to T cell area -> APCs present antigen and deliver other activation signals (like cytokines)

80
Q

CAM

A

Cell Adhesion Molecules
- chemokine receptors on T cell surface bind chemokines expressed/released by other cells

81
Q

CAMs mediating cell-cell interactions

A

different CAMs mediate cell-cell interactions
- naive T cell with HEV
- T cell with APC
- Effector T cell with target cells

82
Q

T cell contact with APC

A
  1. T cells contact APCs using CAMs
  2. TCR scans APC-MHC complexes
    no recognition -> disengages
    recognition -> CD3 signal from TCR complex
    - increases affinity for CAM interactions
    -> T cell divides -> differentiate into effector cells -> exit lymph nodes
    -> T cell- mediated response
83
Q

Signals T-cells require to be activated

A

LFA-1: Leukocyte Function associates Antigen
ICAM-1: InterCellular Adhesion Molecule

84
Q

three signals needed for T-cell activation

A

Signal 1: from TCR contacting MHC/ peptide on APC
Signal 2: APC also express co-stimulatory molecules that bind CD28
Signal 3: APCs release cytokines -> bind to cytokine receptors

85
Q

T cells activated by 3 signals ->

A

proliferate and express ICOS and CTLA-4
- ICOS binds ICOL on APC -> cytokine secretion
- CTLA-4 binds B7.1/2 on APC -> negative signal to activated T cell -> dampens down/limits T cell response

86
Q

PRR

A

Pattern Recognition Receptor
- Expressed by APCs
- binding -> activates APC

87
Q

APCs

A

express MHC class I and II molecules
Dendritic cells-> present Ag, activate naive T cells
Macrophages and B cells

88
Q

Myeloid cells

A

(coventional DC 2/3)
- potent APC involved in activation of naive T cells
- dont express co-stim molecules until active
- mature and migrate to lymph node after danger signal

89
Q

Plasmacytoid

A

(pDC, DC6)
- viral infection
secrete a and b interferons
express TLR 7 and 9 -> snese viral antigens

90
Q

Maturation of dendritic cells

A
  1. immature dendritic cells are activated by PAMPs
  2. TLR signalling induces CCR7, enhances antigen processing
  3. CCR7 directs migration into lymphoid tissues, augments expression of co-stim and MHC molecules
  4. mature dendritic cell in T cell zone primes naive T cell
91
Q

IL-2

A

key cytokine for T cell survival - potent autocrine T cell growth factor
IL binding to IL2R on activated T cells
-> T cell proliferation

92
Q

After activation by APC, T cells differentiate into:

A

effector T cells
- CD8+ cells acquire cytotoxic activity
- CD4+ cells function by secreting cytokines

93
Q

Effector T cells

A

display effector function when TCR engaged
- no longer require co-stim
- change expression of adhesion molecules
no longer enter lymoh nodes
but still enter tissues
-> migrate to where they are needed

94
Q

activation of CD8+ T cells

A

requires high levels of co-stim activity
- CD8+ T cells can be activated directly by infected/cross-presenting APC
- may require additional help from CD4+ T cells

95
Q

antibody functions

A
  1. neutralisation - prevents bacterial adherence
  2. opsonisation - promotes phagocytosis
  3. complement activation
96
Q

BCR signal 1

A

crosslinking of BCR -> activates intracellular kinases

97
Q

enhancing B cell signal 1

A
  • if it has activated complement cascade -> lots of C3b
  • complement receptor 2 on B = CD21
  • CR2/CD19/CD81 -> form complex -> augments the signal
98
Q

BCR TI Ag signal 2

A

Thymus-independent Ag
- signal 2 is provided by the antigen itself or by BCR cross-linking

99
Q

BCR TD Ag signal 2

A

Thymus dependant Ag
- signal 2 provided by CD4+ T cells

100
Q

TI antigen

A

Thymus independent
- antibody production without needing T cell involvment

101
Q

TI-1 Ag

A

Binds BCR etc -> signal 2
- in high concs, act as mitogens (polyclonal activators) for B cells
- the two signals (1 from BCR, 1 from TLR) -> B cell activation/proliferation/Ab secretion

102
Q

TI-2 Ag

A
  • repeated epitopes
  • cross link many BCR on same cell
  • induce B cell activation
    Don’t develop until 5 years old
103
Q

TD Ag

A

Requires presence of CD4+ cells
- Ab responses much better than Ti
- CD4+ cells -> recieve signal 2 via CD40 interaction
- can help induce Ig class switching

104
Q

Way to improve efficency of a vaccine

A

converting TI Ag to TD Ag (conjugate vaccine)

105
Q

Germinal centre

A

where lots of B cells are proliferating
-> centroblasts
-> centrocytes

106
Q

B cell zone

A
  • in lymph node
    dark zone: loads of cells proliferating
    light zone: less cells
    FDC: follicular dendritic cells
107
Q

B cells withing a GC

A
  1. Differentiate into plasma cells
  2. form long-lived memory cells + recirculate
  3. Die within lymphoid tissue if BCR no longer binds antigen
108
Q

FDCs

A

Follicular dendritic cells
- not derived from bone marrow
- capture intact Ag for centrocytes to bind via BCR

109
Q

Follicular T helper cells

A

CD4+ cells in B cell folicles of lymph node
- secrete Th1 and Th2 cytokines

110
Q

role of CD40 on B cells

A
  • protects centrocytes from apoptosis
  • induces isotype switching
111
Q

why do we need immunological tolerance?

A
  • random BCR/TCR repertoire -> some self reactive
  • no tolerance -> autoreactivity -> serious pathology
112
Q

AIRE

A

autoimmune reglator protein
- transcription factor, key role in tolerance induction
deficiency -> major autoimmune syndrome

113
Q

Tolerance through clonal anergy

A

lymphocytes that regognise self-ag can become unresponsive
- important for generating peripheral resistance

114
Q

immunological tolerance

A

many Ag not presented at sufficent levels to activate T cells

115
Q

Regulatory T cells

A

CD4+ subset that suppress immune responses
- crucial for preventing autoimmune responses
- arise in thymus from T cells with high affinity receptors for self -Ag
- produce IL-10/TGF-b -> inhibit self-reactive cells

116
Q

Regulatory B cells

A

B cells that secrete IL-10
- prevent autoimmunity

117
Q

Th1

A

activation of macrophages, NK cells, cytotoxic T cells
respond to IC pathogens

118
Q

Th2

A

promote eosinophil/mast cell mediated/ antibody responses - esp IgE
- respond to EC parasites

119
Q

Th17

A

recruit neutrophils against fungi
secrete IL-17

120
Q

Tfh

A

helps B cells
can produce Th1,2,17 cytokine

121
Q

CD4+ Th1 can kill…

A

chronically infected macrophages
via Fas ligand
-> bacteria is released and destroyed by other, healthy macrophages

122
Q

CD4+ Treg

A

CD4+/CD25+
nTreg = from thymus
iTreg = from circulation
- secrete suppressive cytokines

123
Q

gram positive bacteria

A

thick layer of peptidoglycan

124
Q

gram negative bacteria

A

thinner peptidoglycan layer, outer membrane

125
Q

binding of PAMP to TLR ->

A

promote inflammation
promote dendritic cell maturation
influence differentiation of t cells
activate B cells

126
Q

virus infected host cells

A

type one interferons - IFN-a, IFN-b
- prevents viral nucleic acid production + replication

127
Q

IFN induces synthesis of

A

2,5-oligoadenylate synthetase -> degrades viral mRNA
protein kinase -> inhibits protein synthesis

128
Q

type 2 interferon

A

IFNy - secreted by T cells and NK cells
- recruits Th2 response, promotes Th1
- recruits macrophages

129
Q

Natural killer cells

A
  • innate lymphoid cells
  • recognises stressed cells in absence of Igs and MHC
130
Q

what do NK cells kill with

A

perforin and granzyme
- EC mechanism

131
Q

perforin

A

cytotoxic granule - polymerises in membrane

132
Q

granzymes

A

cytotoxic protease that enters cell

133
Q

killing by cytotoxic T cell

A
  1. secretion of cytotoxic granules: perforin and granzymes
  2. Fas ligang on T cell interacts with Fas on target -> death
    -> apoptosis
134
Q

4 mechanisms pathogens use to evade immunity

A
  • concealment of antigens
  • antigenic variation
  • immunosuppression
  • interference with effector mechanisms
135
Q

concealment of antigens

A

some viruses inhibit antigen presentation by MHC I via privileged sites and uptake of host molecules (cloak effect)

136
Q

4 mechanisms of antigenic variation

A
  1. large number of antigenic types
  2. mutation = antigenic drift
  3. recombination = antigenic shift
  4. gene switching
137
Q

streptoccocus pneumoniae

A

-> otitis media, sinusitis, bronchitis, pneumonia
gram positive
antibodies to the capsule opsonise bacteria and protect
- large number of different capsular types

138
Q

pneumovax

A

vaccine for s.pneumoniae
- polysaccharide vaccine - antigens to all 23 capsules
- not effective in children under 2 or immunocompromised people -> just B cell IgM

139
Q

Prenvar 13

A

vaccine for s.pneumoniae
- conjugate vaccine - only 13 capsule antigens bound to diptheria toxin - highly immunogenic but non-toxic
- T cell and B cell (all Ig) response
- converts TI-2 ag -> TD ag == young children can respond

140
Q

B&C influenza virus

A
  • RNA virus w/ -ve sense segmented genome
  • major surface antigens: haemagglutin and neuraminidase
  • can undergo antigenic drift and shift
141
Q

antigenic drift ->

A

mild epidemic

142
Q

antigenic shift ->

A

major pandemic

143
Q

trypansoma brucei

A

protozial parasite -> african sleeping sickness
- genetic rearrangement -> changes in major surface antigens of trypanosome

144
Q

immunosuppression

A
  1. infection of immune cells
  2. induction of regulatory T cells
145
Q

Helicobacter pylori

A

gram negative -> gastric/duodenal ulcers -> gastric adenocarcinomas
- Treg cells may be involved -> persistent infection

146
Q

measles virus

A

RNA virus -> disease w/ rash/malaise/resp distress
infects dendritic cells -> increased apoptosis, decreased t cell stimulation, decreased IL-12 production

147
Q

molecules interfering with antibody function

A

IgA proteases
Fc-binding molecules

148
Q

molecules interfering with complement

A

pseudomonas -> enzymes that break down C3a/C5a
molecules inhibiting complement activation

149
Q

IL-1b effects

A

local: activates vascular endothelium and lymphocytes, local tissue destruction, increased acces of effector cells
systemic: fever, IL-6 production

150
Q

TNFa effects

A

Local: increased vascular permeability -> increased entry of IgG complement and cells to tissues, increased lymph drainage
Systemic: fever, shock, mobilization of metabolites

151
Q

IL-6 effects

A

local: lymphocyte activation, increased antibody production
systemic: fever, induces acute phase protein production

152
Q

CXCL8 effects

A

Local: chemotactic factor, recruits neutrophils, basophils and T cells to site of infection

153
Q

IL-12 effects

A

Local: activates NK cells, inducing CD4+ cells -> Th1 cells

154
Q

local infection with gram-negative bacteria

A

-> macrophage secrete TNFa into tissue
-> release of plasma proteins and lymphocyte migration, increased platelet adhesion to blood vessel wall
-> bacteria phagocytosis, local vessel occlusion, plasma and cells drain to local lymph node
-> removal of infection, adaptive immunity

155
Q

Sepsis

A

overreaction of immune system
systemic infection -> sepsis -> mass cytokine release -> death

156
Q

cytokine storm

A

shed glycoprotein from virus binds macrophage and dendritic cells -> cytokine release -> increased vascular permeability

157
Q

immuno pathology

A
  • cytokine storm
  • coagulation cascade
    disseminated invtravascular coagulation -> death
158
Q

passive immunity

A
  • short lived half life ~ 3wk
159
Q

Active immunity

A
  • exploits immunological memory
  • secondary response is faster and greater than primary response
160
Q

requirements of a safe and effective vaccine

A

safe
high level of lasting protection
right type of response
low cost
stable
easy administration
minimal side effects

161
Q

inactivated vaccines

A

dead organisms

162
Q

attenuated vaccine

A

live but virulence disabled
e.g. yellow fever and BCG vaccine, MMR, vaccina, sabin

163
Q

subunit vaccine

A

protein fragments
e.g. hepatitis B

164
Q

Toxoid

A

bacterial toxin
e.g. tetanus

165
Q

conjugate vaccine

A

something with low antigenic property covalently bound to something with high
e.g. s.pneumoniae + diptheria

166
Q

pros and cons of live vaccines

A

pros: single dose, may be given by natural route, may induce local/systemic immunity, may induce right type of response
cons: reversion to virulence, contamination possible, susceptible to inactivation, causes disease if host is immunocompromised

167
Q

Adjuvants

A

= substance administered with an antigen to promote immune response
- pure antigens only elicit a weak response, adjuvants enhance these responses

168
Q

ways that adjuvants can act

A
  • activate and promote uptake by dendritic cells
  • release endogenous danger signals
  • stimulate release of cytokines/chemokines
  • promote cross-penetration of exogenous antigens
169
Q

animal adjuvants

A

freud adjuvants: oil in water emulsion
freud complete adjuvants: also contains mycobacteria

170
Q

human adjuvants

A
  • aluminium most commonly used
  • aluminium hydroxide/phosphate
  • better Ab responses than cell mediated immunity
171
Q

antiserum

A

serum from an immunized person/animal
- contains antibodies that will bind the Ag

172
Q

limitations of using antisera

A
  • would be v useful if purified, but contains a mixture of Abs

Biomed year 2 sem 1 (7 decks)

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