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M1 Immunology > Adaptive Immunity > Flashcards

Adaptive Immunity Flashcards

1
Q

Which antigen presentation pathway is used in a viral infection?

A

MHC1 to CD8+ Tc cells

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2
Q

Which antigen presentation pathway is used in an bacterial/parasitic infection?

A

MHC2 to CD4+ Th cells

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3
Q

Which cells present antigens via the MHC1 pathway?

A

all nucleated cells

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4
Q

Which cells present antigens via MHC2 pathway?

A

Macrophages, Dendritic cells and B cells

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5
Q

Which cell links the innate and adaptive arms of the immune reponse?

A

Dendritic cells

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6
Q

Where do Dendritic cells go after phagocytosing microbes?

A

lymph nodes

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7
Q

Where do T cells encounter/interact with DCs?

A

In lymph nodes

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8
Q

How are T cells positively selected?

A

T cells enter lymph nodes across HEVs in the cortex
- Non-Ag specific → leave through efferent lymphatics
- Ag-specific → proliferate and differentiate into effector cells

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9
Q

How is the T cell-DC interaction in lymph nodes extended/mediated?

A

1) Initial contact low affinity:
LFA-1(T cell):ICAM-1(APC)

2) TcR:MHC2 interaction → conformational change of LFA-1 → ↑ affinity → prolong cell-cell contact

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10
Q

What are the 3 signals in T cell activation?

A

1) Specific signal (Specific TcR→peptide)
2) Co-stimulatory signal (CD28-B7)
3) Cytokines → differentiation

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11
Q

Other than the 3 signals, how else is T cell activation controlled?

A

Activating and inhibitory receptors

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12
Q

What happens if all 3 signals are not present?

A
  • Only 1: Anergy
  • Only 2: no effect
  • Only 1 and 2: no differentiation/not effector
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13
Q

What are 3 changes in T cells after activation?

A

1) ↑ exp. of CTLA-4 → ↓ APC adhesion
2) ↓ exp. of CCR7 & L-selectin → ↓ endothelium adhesion
3) S1P gradient → S1PR-1 receptor on T effector cells → chemotaxis to infection sites

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14
Q

What is CD3?

A

The signalling component of in T cell membranes common to both CD4+ and CD8+

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15
Q

What are the steps in intracellular signalling in activated T cells upon TcR-MHC binding?

A

1) CD4/8 recruit ITAMs
2) LCK (kinase) phosphorylate ITAMs
3) LCKs phosphorylate ZAP-70 → downstream signalling → regulate transcription factors

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16
Q

How does IL-2 binding differ in a resting and activated T cell?

A

Activated T cells have an additional α subunit in the IL-2R (α,ß,y)
→ secrete more IL-2 (+feedback/autocrine loop)
→ clonal expansion

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17
Q

What are CD8+ T cells?

A

CTLs/Cytotoxic effector cells

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18
Q

How are CD8+ T cells activated?

A

1)They recognise intracellular pathogens/ peptides displayed on MHC 1
2) Co-stimulation by CD28:B7
3) IL-2 from CD4+ Th cells

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19
Q

Other than signal 1-3, what is needed for fully functional CD8+ T cells responses?

A

CD40 & 4-1BB exp. on APC (by CD4+ Th cells)
→ co-stimulate CD8+ Tc cells
(by binding to CD-40L and 4-IBBL on T cells respectively)

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20
Q

What are 3 ways in which CD8+ cytotoxic effector cells kill cells?

A

1) Perforin (forms pore)/Granzymes (activates pro-caspase 3
→ binds to iCAD
→ activate CAD
→ CAD cleaves DNA
→ apoptosis)

2) Fas (on target)/FasL (on CTL)
→ activation of caspase 8
→ mitochondrial swelling
→ cytochrome C egress
→ activation of caspase 3 and CAD
OR
→ activate caspase 9
→ activate caspase 3 and CAD

3) TNF α/ß
→ cross-link surface receptors
→ induce apoptosis

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21
Q

How many subsets do we need to know for which a naive CD4+ T cell can differentiate into?

A

5
1) Tfh
2) Th1
3) Th2
4) Th17
5) Treg

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22
Q

How are Th1 cells activated/differentiated?

A

Microbes phagocytosed by Macrophages and DCs → secrete IL-12
→ Il-12 activate NK
→ NK secrete IFN-y
→ Th1 differentiation

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23
Q

What cytokines do Th1 produce?

A

IFN-y

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24
Q

What cells do Th1 activate?

A

M1 (proinflammatory) macrophages

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25
Q

What are the functions of M1 macrophages?

A

1) Proinflammatory (↑MHC, ↑B7)
2) ↑ Microbicidal (↑ ROS and NO, ↑ lysosomal enzymes)
3) Inhibit Th2 (IFN-y)

26
Q

How are Th2 cells activated/differentiated?

A

via IL-4 secretion by mast cells, eosinophils, basophils

27
Q

What cytokines do Th2 produce?

A

IL-4/13 → IgE class switching
IL-5 → Eosinophil activation

28
Q

What cells do Th2 activate?

A

Eosinophils
M2 (anti-inflammatory) macrophages

29
Q

What are the functions of M2 macrophages?

A

1) Anti-inflammatory (IL-10, TGF-ß)
2) Wound repair and fibrosis (TGF-ß, Proline polyamines)

30
Q

What cytokines do Th17 produce?

A

IL-17 A/F → enhance antimicrobial peptides + recruit neutrophils and monocytes
IL-22 → maintain epithelium

31
Q

What is the function of Tregs?

A

Suppress immune response

32
Q

How to Tregs suppress immune responses?

A

1) Constitutive expression of CTLA-4 → sequester and down regulate B7 on APC
2) Inhibitory cytokines eg. TGF-ß
3) Metabolic disruption
4) Cytolysis
5) Modulation of DC maturation/function

33
Q

How to T cells differentiate into memory T cells?

A

1) one of 3 outcomes when a naive T cells sees and antigen and activates
- Central memory T cell → remain in lymphoid tissue
- Effector memory T cell → remain in peripheral tissues

2) The fate of effector T cells alternative to dying
- Quiescent memory cell w CD45R0)

Other than
1) expressing CCR7 and remaining in lymphoid tissues
2) Differentiating into Effector T cells

34
Q

Why do memory cells mount a faster response with higher magnitude upon re-infection?

A

Pre-existing lymphocytes with TcR/BcR/Abs specific for the Ag, ready to undergo clonal expansion

35
Q

What are 3 reasons for declining T cell responses with age?

A

1) Thymic involution (↑age → ↓thymic output)
2) Replicative senescence/Hayflick’s limit
3) T cell oligoclonality (↓diversity of T cell repertoire)

36
Q

What are the 5 types of antibodies?

A

IgM (1st in infection, Monomer or Pentamer)
IgG (Most abundant, can cross placenta)
IgA (Mucosal)
IgE (Type 1 Hypersensitivity)
IgD (Ag receptor on mature but inactivate B cells, activate mast cell and basophil to produce antimicrobial factors)

37
Q

What are the functions of IgA?

A

1) Mucosal immunity (prevent binding of pathogens to mucous membranes)
2) Neutralisation
3) Opsonisation
(also primary Ig in breastmilk and protects baby <2 y/o)

38
Q

What are the functions of IgE?

A

1) Mast cell degranulation (has Fc Region specific to Mast cells FcεR1)
2) Anti-parasitic (has variable region specific to allergens and parasite surface antigens)

39
Q

What are the functions of IgG?

A

1) Pathogen neutralisation
2) ADCC (FcR or Fcy binding)

40
Q

What are the functions of IgM?

A

1) Complement activation (recruit C1)
- low affinity, high avidity

41
Q

Which Ab(s) mediate complement activation?

A

IgM

42
Q

Which Ab(s) mediate immune complex formation?

A

IgM, IgG

43
Q

Which Ab(s) mediate opsonisation?

A

IgG

44
Q

Which Ab(s) mediate neutralisation?

A

IgG, IgA

45
Q

Which Ab(s) mediate ADCC?

A

IgG

46
Q

Which Ab(s) mediate mast cell degranulation?

A

IgE

47
Q

How does immune complex formation aid in adaptive immunity to pathogens?

A

IgM and IgG use multi-bi-valent binding sites → formation of large complexes
→ prevent dissemination
→ promote digestion by phagocytotic cells in spleen/liver

48
Q

How does IgM-mediated complement activation aid in adaptive immunity to pathogens?

A

IgM recruits complements through the classical pathway
→ C1 binds to Fc region of IgM attached to pathogen
→ initiate complement cascade
→ formation of membrane attack complex (C5-9)
→ cytolysis

49
Q

How does opsonisation aid in adaptive immunity to pathogens?

A

IgG coats pathogen and
1) express receptors for FcRs
2) Pro-inflammatory signaling → ultra-aggressive phagocytosis (<10 fold rate of bacterial phagocytosis)

50
Q

How does neutralisation aid in adaptive immunity to pathogens?

A

IgG (blood) / IgA (mucosa) bind to pathogen surface/toxins → block binding to receptors (receptor antagonism)
- most effective way to shut down an infection

51
Q

How does ADCC aid in adaptive immunity to pathogens?

A

IgG binds to antigen → recruits NK cells with CD16R
→ crosslinking of CD16 → degranulation
→ lytic synapse → apoptosis

52
Q

What is the difference between affinity and avidity?

A

Affinity is the strength of binding between 1 paratope and 1 epitope
Avidity is the strength of binding between multiple repeating epitopes on 1 Ag and 1 Ab

53
Q

How are the light and heavy chains of an antibody held together?

A

Inter and intrachain disulfide bonds

54
Q

How is diversity in Abs achieved?

A

1) Random silencing of LC gene loci (Chromosome 2/22)
2) Random stitching of DNA segments coding for light chains
3) VDJ recombination of heavy chains
4) Somatic hypermutation by AID
5) Cytokine-induced class switching

55
Q

What is the process of B cell development in the bone marrow?

A

1) Haematopoietic stem cell → lymphoid progenitor → B cell
2) IgH gene rearrangement → pre-BCR
3) Positive selection for functional VDJ heavy chains (receive +survival signal)
4) IgL gene rearrangment → BCR (IgM)
5) Negative selection for autoreactivity → naive B cells released to circulation

56
Q

Is B cell isotype switching reversible or irreversible?

A

Irreversible

57
Q

Using IgM → IgE as an example, explain the process of B cell isotype switching.

A

1) Initial μ gene exp. → IgM
2) Th2-B cell interaction → IL-4
3) Looping + excision of μ to y4 (in Ab Fc region) of DNA
4) DNA rearrangement/ligation
5) ε gene exp. → IgE

58
Q

Where does affinity maturation of B cells occur?

A

germinal centers of secondary lymphoid organs (eg. lymph nodes)

59
Q

Explain the process of B cell affinity maturation.

A

1) Somatic hypermutations via activation-induced deaminase (AID) [DARK ZONE]
→ insert base mismatches (C→U) → multiple potential outcome of repair
→ ↑↑point mutations in variable regions → ↑ variety of affinity

2) Competition for Iccosomes from FDC [LIGHT ZONE]
→ B cells with BCR specific for Ags in Iccosomes
→ bind and tear off iccosome somes → internalise and present via MHC2

3) Activation by CD4+ Th cells/ +ve selection [LIGHT ZONE]
→ Ag:TcR interaction + CD40:CD40L co-stimulation → cytokine secretion
→ cytokine determines B cells differentiation (plasma or memory B cell)

60
Q

How does the lower dose vaccines and progressive infection produce a stronger immune response?

A

Later in infection/lower dose → ↓Ag → ↑Competition for Iccosomes
→ only those with ↑ binding affinity have ↑ chance of acquiring iccosomes
→ only B cells with better BcR/Abs can present to Th cells and receive survival/differentiation/proliferation signals

61
Q

What is the name for a B cell in the dark zone of a germinal center?

A

Centroblasts (black blasts)

62
Q

What is the name for a B cell in the light zone of a germinal center?

A

Centrocytes (cytes, sights, see, light)

M1 Immunology (9 decks)

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