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Paper 4 > Immunology > Flashcards

Immunology Flashcards

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1
Q

Over immune system

A
  • Costly
  • Well balanced
  • Infectious agents spectrum
  • Self from non-self
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2
Q

Components of immune system

A
  • Myleoid stem cells
  • Lymphoid stem cells
  • Dendritic cells bridge innate + adaptive systems
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3
Q

Innate vs adaptive immune systems

A
  • Innate = 1st line of defence, rapid

- Adaptive = 2nd, slower but specific

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4
Q

Major histocompatibility complex

A
  • Genetic locus, 3000kb
  • Encodes MHC class I + II
  • Similar = receptor for foreign peptide
  • Polymorphic
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5
Q

MHC class I

A
  • a chain 450kDa, B2 micro globulin
  • Membrane-distal (a1 + a2)
  • Peptide binding groove (defines groove but degenerate)
  • Foreign protein denatured 7-9aa fragment
  • All somatic cells have
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6
Q

MHC class I endogenous pathway

A
  1. Proteosome = 700kD, 15-20 enzymes

2. Transporter associated w/ antigen processing (TAP) = translocates small peptides across membrane

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7
Q

MHC class II

A
  • Restricted to APCs
  • a chain (33kD) and B chain (28kD), each folds to 2 domains
  • Have peptide binding groove
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8
Q

MHC class 2 endocytic pathway

A
  • Ag matures → late endoscope
  • Environment ↑ acidic, degrades protein
  • MHCII assembled in ER
  • MHCII intersects endocytic pathway at late endosome
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9
Q

Recognition of foreign Ag (T cells)

A
  • Important in adaptive immune response
  • T cell = leukocyte
  • Activated T cells by recognition of specific ligand through TCR
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10
Q

TCR

A
  • Composed of 2 chains, a and B, 40-50kD

- Peptide binding to MHC recognised by TCR

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11
Q

TCR diversity

A
  • Problem with diversity (diverse ligands, MHC polymorphic, peptide to MHC binding is degenerate)
  • Solution (TCRs differ in membrane distal portion, 10^9 versions of TCR)
  • Generating diversity (a+b composed of various regions encoded by separate genes, a = v,j,c b = v,j,c,d, randomly combine v,j,c,d, excise intervening DNA, a pairs w/ b → 10^9-10^16 different TCRs
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12
Q

T cell types

A
  • CTL = made in thymus, express TCR + CD8, recognise MHCI, needed for defence against IC pathogens
  • Th1 = responds to IC pathogens, has CD4+, secretes IL-2 that activates macropgage
  • Th2 CD4+, humeral immunity, EC organisms, produces activation signals like IL-10 to proceed Ab
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13
Q

CTL response

A
  1. Secretion of cytokines (TNFa + IFNy)
  2. Production + release of cytotoxic granules
    - Perforin + granzymes
  3. Destruction of infected cells w/ Fas/FasL (activated CD8+ express FasL, binds Fas → Fas trimerises → caspase cascade, CD8+ express Fas + FasL so can kill each other in contraction phase)
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14
Q

Immunoglobulin

A
  • Bridges adaptive + immune system
  • V(D)J recombination, need to recognise ↑ Ag
  • Heavy chain of Ig = v,d,j,c light chain = v,j,c
  • Somatic hypermutation, clonal expansion, changes affinity
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15
Q

Immunoglobulin repsonse

A
  1. Neutralisation
  2. Opsonisation (coat pathogen w/ complement factors, assists phagocyte binding, or fab portion of igG Ab binds to Ag, Fc of Ab binds FCR which traps organism at surface + stimulates phagocytosis)
  3. Complement fixation (innate defence, classical = triggered by activation of C1 by C1q binding to Ch3 of IgM or Ch2 of IgG, C1q binds at least 2 Ig Fc)
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16
Q

Lymphoid organs

A
  • Naive T/B confined
  • Io/2o organs
  • Functions of 2o lymphoid organs (overcomes unfavourable odds of T/B encountering specific Ag)
  • Rapidly screen repertoire + see appropriate clones
  • Disadv = time needed to identify + expand relevant clones leaves host vulnerable
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17
Q

Acute inflammatory response

A
  • Innate immune system transports Ag from infection to lymphoid to present to T/B cells via inflammatory immune response
  • Limits spread of infection
  • Infectious microorganism = detected by PRR + NCR
  • These receptors = invariant
  • Diff TCRs bind diff PAMP
  • Inflammation = triggered by damaged cells or basophils → local changes at site of infection (vasodilation, ↑ vascular permeability)
18
Q

Complement system role

A
  • w/o Ig, use alternative pathway
  • C5a = chemoattractant, causes secretion of elastase
  • Lysis of bacteria
  • Opsonisation
19
Q

Microbial killing

A
  • Mø undergoes respiratory burst

- Kills internalised cell by O2-dependent mechanism

20
Q

Dendritic cell

A
  • Immature DCs = acquire Ag by phagocytosis + endocytosis
  • In response to inflammation, x phagocytose
  • Migrate to lymph nodes, mature (Cd40/86)
  • Span adaptive and innate
21
Q

TLR

A
  • Receptors for MAPM
  • MAPM include dsRNA, LPS, flagellin
  • Bind TLR
22
Q

T-B cell cooperation

A
  • B cells = like APC but use specific Ig
  • Th2 activated (MHC on DC) and then migrates to B cell
  • Recog. of same peptide-MHC → secretion of cytokine → activate B cell → ↑ secretion of Ig
23
Q

Cost of immune system

A
  • Specific for self + foreign Ag
24
Q

Self tolerance

A 
Innate = Ag receptor = germline encoded, use non-protein Ag, response inflexible 
Adaptive = receptors rearranged, response is flexible
25
Q

T cell differentiation

A
  • Mature in thymus
  • 4 subsets of thymocyte
  • Interactions w/ stroll cell cells → thymocyte along a diff pathway
26
Q

T cell diff checkpoints

A
  1. Transition from CD4-8- to CD4+8+
    - Express product of gene rearrangement expressed at surface w/ pre-TCR a antigen
    - Ligantion of pre-TCR by ligand signals to thymocyte B chain is functional → a chain rearrangement can start
  2. Transition from CD4+8+ → mature CD4+8- (Th cell) or CD4-8+ (CTL)
    - Involves +ve selection
    - TCRs that complement shape of MHC molecule = +ve
    - If x fit die by neglect
    - -ve selection
    - Screen cells w/ functional TCRs for self reactivity

Paradox

  • +ve selection ensures MHC-restricted recognition
  • -ve selection ensures cells are self-tolerant
  • Both involve ligation of TCR by complexes btw self-peptide + MHC determinant
  • Same ligand recognised by same TCR but → diff outcome
27
Q

Differential affinity model

A
  • Avidity of Ag recognition = to do w/ affinity for self-peptide-MHC
  • x affinity = dies
  • Too high = deleted by DC
28
Q

Issues w/ -ve selection

A
  • Self-components may x be present (developmental Ag, immunologically-privileged sites)
  • Can release sequestered self compounds
  • Cross-reactivity btw self components + infectious agents → molecular mimicry
29
Q

Myasthesia Gravis

A
  • Muscle weakness
  • Ab for AchR
  • Binding of Ab to AchR means Ab compete w/ Acc for binding → functional blockade → x open → x muscle contraction
30
Q

Antigen presentation (extra)

A

MHC I

  • Peptide translocated to ER by TAP
  • Peptides bind MHC I, chaperone are released, MHCI leaves ER

MHC II

  • Cathepsin S + L are activated + digest MHC Class Ii → CLIP
  • CLIP exchanged for antigenic peptide derived from protein in eadosomal pathway
31
Q

NK vs CD8 cell

A
  1. Recognition
    - CD8 = single TCR, NK = several (inhibitory + activator)
    - Missing self recognition (MHC I switches off NK cell)
    - CD8 needs CD80/86 or CD28
    - CD28 needed for cytokine secretion + proliferation in NK cells
    - T cells also need pro-inflam. cytokines
  2. Destroying cells
    - Perforin + granzymes
    - Both have FasL
    - CTL = stable contact w/ target, NK forms transient
    - NK have more perform, CD8 have more granzyme B
    - NK have cytotoxic granules already, CD8 x (memory do)
  3. Memory
    - CD8 undergo contraction, 5% remain → memory T
    - Faster 2o response
    - NK cells undergo contraction
    - NK memory x as stable, NK cells decay at same rate
32
Q

How ‘self’ Ag arise

A
  • Body needs ↑ diverse immune
  • Random re-arrangement
  • Random → specificities that recog. own
33
Q

Central tolerance (T cell)

A
  • 1o lymph tissues
  • T cells / low affinity for self MHC → diff to CD4 or CD8 single +ve (+ve selection)
  • High affinity TCR for self-MHC die
  • If x bind die
  • Zipper model (zipper btw membrane-proximal domain of CD8B + peptide of a chain of TCR)
34
Q

Central tolerance (Aire)

A
  • Some peptides expressed in other cells
  • AIRE in thymic medulla induces expression of ↑
  • ↑ efficiency of -ve selection
  • APECED
35
Q

Central tolerance (B cell)

A
  • Auto-reactive → auto-Ab → autoimmune
  • Strength of BCR to Ag
  • If weak leave bone marrow
  • Tolerance x as strong, help from T helpers
36
Q

Clonal deletion

A
  • 2/3 of T cell
  • Fas-FasL apoptosis
  • Nur77 + Bim
37
Q

Peripheral tolerance

A
  • Some Ag are seen w/ inadequate affinity or have too ↓ conc
  • Tolerance needs to be incomplete
38
Q

Peripheral tolerance (T cell)

A
  • Intrinsic = T cell anergy, phenotype skewing

- Extrinsic = reg. by Treg cells

39
Q

Peripheral tolerance (B cell)

A
  • Somatic mutation → B cell w/ new Ag specificities

- Th for activation

40
Q

Anergy

A
  • Cells x killed but inactive
  • Following peptide + MHC engagement for T cell or free epitope engagement for B cell
  • Absence of co-stim receptor activates NFAT, w/o APA-1
41
Q

Tregs

A
  • FoxP3
  • Natural / induced Tregs
  • Regulate effector T by ↑ mechanisms
  • Tregs down-reg. APC function by CTLA-4-dependent mechanism
  • Secrete immunosuppressor molecules
  • Maintain population

Paper 4 (31 decks)

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