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CA1 Extra Qns > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the role of neutrophils?

A

Neutrophils engulf bacteria and fungi, first cells to respond to infection
- produced by bone marrow
(neutropenic patients are at high risk of septicaemia -> septic shock)

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2
Q

What is the role of eosinophils?

A

Eosinophils defend against parasites, mediates hypersensitivity type I reactions

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3
Q

What is the role of macrophages?

A

Macrophages engulf bacteria and fungi, can survive in the sites for a long time
- antigen presenting cell

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4
Q

What is the role of dendritic cells?

A

Phagocytic cells that are activated by binding of PAMP to PRR and cytokine signalling.
Upon engulfing pathogens, process and display their constitutent antigens on MHC II to activate the adaptive immune system

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5
Q

What is the role of natural killer cells?

A

They recognise and kill infected and stressed cells by antibody-dependent cellular cytotoxicity
- involved in viruses

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6
Q

Peptide on MHC class I is presented to…

A

CD8 T cells

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7
Q

Peptide on MHC class II is presented to…

A

CD4 T cells

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8
Q

What is important for naive T cells entering the peripheral lymphoid organs?

A

CCR7 and L-selectin

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9
Q

What leads activated T cells out of lymph nodes to site of infection?

A

S1P gradient

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10
Q

Co-stimulatory molecules expressed on _______ are ___ molecules which bind to _________

A

Co-stimulatory molecules expressed on antigen-presenting cells are B7 molecules which bind to CD28 on T cells

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11
Q

Both specific antigen and co-stimulatory molecules on APC must bind to TCR and CD28 on T cells.

Binding of
- co-stimulatory molecule alone: ?
- specific signal alone: ?

A

Binding of
- co-stimulatory molecule alone: No effect on T cell
- specific signal alone: Inactivates T cell

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12
Q

T cell activation through TCR and CD28 leads to increased expression of _____ which is an ___________

A

T cell activation through TCR and CD28 leads to increased expression of CTLA-4 which is an inhibitory receptor for B7 molecules

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13
Q

Agonist antibodies will _____ activating receptors on T cells

A

Agonist antibodies will activate activating receptors on T cells

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14
Q

Blocking antibodies will _____ inhibitory receptors on T cells

A

Blocking antibodies will inhibit inhibitory receptors on T cells

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15
Q

What does Lck phosphorylate during antigen recognition by T cells?

A

Lck phosphorylates ITAM and ZAP-70

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16
Q

What is the process of clonal expansion?

A
  1. Resting T cells express moderate-affinity IL2 receptor
  2. Activated T cells express high-affinity IL2 receptor and secretes IL2
  3. IL2 binds to its receptor and signals T cell to enter cell cycle
  4. IL2 induces T cell proliferation
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17
Q

What induces T cell proliferation?

A

IL2

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18
Q

What are the effector subsets of naive CD4+ T cells? And what cytokines do they secrete?

A

Th1 (IFN-gamma)
Th2 (IL4, IL13)
Th17 (IL17a, IL17f)

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19
Q

Native CD4 T cells activated in the presence of IL12 (by dendritic cells) and IFN-gamma (by NK cells) will differentiate into…

A

Th1 cells

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20
Q

Native CD4 T cells activated in the presence of IL4 will differentiate into…

A

Th2 cells

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21
Q

What do activated Th2 cells secrete?
What is the function?

A

TGF-beta and IL10
inhibit Th1 proliferation

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22
Q

What do activated Th1 cells secrete?
What is the function?

A

IFN-gamma
inhibit Th2 proliferation

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23
Q

Central memory T cells remain in…

A

lymphoid tissue

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24
Q

Effector memory T cells reside in…

A

peripheral tissues

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25
Q

What is the role of cytotoxic CD8 T cells?

A

It releases:
- perforins: inserted into target cell membranes to form pores
- granzymes: activate apoptosis
- granulysin: induce apoptosis
=> killing intracellular pathogen

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26
Q

What is the role of Th1 cells?

A

Th1 cells activate M1 macrophages:
- releases reactive oxygen species and nitric oxide
- increased lysosomal enzymes
- promote inflammation
- recruit more leukocytes

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27
Q

What is the role of Th2 cells?

A

Th2 releases IL4, IL5, IL13
IL4 and IL13:
- act on B cells for IgE antibodies production -> mast cell degranulation
- intestinal mucus secretion and peristalsis
- alternative macrophage (M2) activation -> tissue repair and fibrosis
IL5:
- eosinophil activation -> destruction of helminths

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28
Q

M1 macrophages are induced by IFN-gamma (released by Th1) and have ____ effects

A

M1 macrophages are induced by IFN-gamma (released by Th1) and have pro-inflammatory effects -> phagocytosis and killing of bacteria and fungi

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29
Q

M2 macrophages are induced by IL4 and IL13 (released by Th2) and have _____ effects

A

M2 macrophages are induced by IL4 and IL13 (released by Th2) and have anti-inflammatory effects -> tissue repair and fibrosis

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30
Q

What is the role of Th17 cells?

A

Th17 secretes IL17 and IL22
- inflammation, neutrophil response
- antimicrobial peptides
- increased barrier integrity (IL22)

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31
Q

What cells do Treg cells inhibit?

A

Treg inhibits Th1 cells

32
Q

What are the 4 types of hypersensitivity responses?

A

Type I: IgE-mediated hypersensitivity
Type II: Antibody-mediated hypersensitivity
Type III: Complex-mediated hypersensitivity
Type IV: Cell-mediated hypersensitivity

33
Q

List the 3 steps in type I hypersensitivity.

A
  1. Sensitization
    First exposure to allergens -> activation of Th2 and Tfh cells -> production of IgE antibodies
    IgE antibodies are tightly bound to the surface of mast cells by IgE receptor FceRI
  2. Activation of Mast Cells and Secretion of Mediators
    Mast cells are sensitised by IgE
    Upon repeated exposure to allergens, cross-linking of allergens on the IgE antibodies -> mast cell degranulation
  3. Late phase Reaction (does not occur in everyone)
    Recruitment of leukocytes + continuous synthesis and release of inflammatory mediators -> delayed inflammation reactions
34
Q

What are the mediators released by mast cells?

A

histamines, proteases, leukotrienes, prostaglandins, platelet-activated factor, cytokines, chemokine

35
Q

What is the effect of the mediators released by mast cells?

A

Increased vascular permeability, Vascular dilation, Tissue damage, Inflammation, Smooth muscle contraction

36
Q

What is type II hypersensitivity?

A

Antibodies bind directly to their target antigens which is fixed on cell surface or in extracellular matrix -> cause tissue injury and inflammation at that specific location

37
Q

What is type III hypersensitivity?

A

Antibodies form immune complexes (antigens floating freely around) and deposit mainly in blood vessels causing vasculitis

38
Q

What is type IV hypersensitivity?

A

could be due to autoimmunity or environmental antigens

inflammation is caused by either CD4 T cell by activated macrophages or CD8 cytotoxic T cells killing target cells

39
Q

What is type IV hypersensitivity?

A

could be due to autoimmunity or environmental antigens

inflammation is caused by either CD4 T cell by activated macrophages or CD8 cytotoxic T cells killing target cells

40
Q

How do tumours evade immune response?

A
  1. They lose the expression of antigens
  2. They produce immunosuppressive cytokines (TGF-beta) or ligands (PD-L1) for inhibitory receptors on T cells
41
Q

How does the chimeric antigen receptor work?

A
  1. remove blood from patient to get T cells
  2. make CAR T cells
  3. grow millions of CAR T cells
  4. infuse CAR T cells back into patient
  5. CAR T cells bind to cancer cells and kill them
    (CAR T cell will bind to CD19 receptor)
42
Q

What is central tolerance?

A

immature lymphocytes undergo selection process in thymus (primary lymphoid organ)
- acts on both CD4 and CD8 T cells

43
Q

Positive selection is…

A

T cells expressing TCR that binds with low to moderate affinity with self-MHC presenting self-peptide will survive and have the potential to bind to MHC + foreign peptide with high affinity

T cells with TCRs that do not bind -> apoptosis

44
Q

Negative selection is…

A

T cells expressing TCR that binds TOO strongly to self-MHC presenting self-peptide -> apoptosis

45
Q

What is autoimmune regulator (AIRE)?

A

AIRE is a transcription factor.
When it is switched on, it allows thymus to express small amounts of tissue-specific antigens
Any TCRs with high affinity for extra-thymic self antigen:self MHC will be eliminated (negative selection)

46
Q

Activation of naive T cells requires:

A
  1. TCR binding to peptide:MHC complex
  2. Co-stimulation (B7 molecules bind to CD28 receptors)
  3. Cytokines from APC
47
Q

What is peripheral tolerance?

A

mechanisms operating on mature lymphocytes in the periphery

47
Q

Differences between central and peripheral tolerance

A

Central tolerance:
- acts in thymus
- acts on immature T cells
- T cells with TCRs that have high affinity for self-peptide:self-MHC complex would be eliminated

Peripheral tolerance:
- acts outside thymus in the periphery
- acts on matured but naive T cells
- T cells that have been inactivated or too weak an interaction between TCR and peptide:MHC complex would be eliminated

48
Q

Differences between CTLA-4 and CD28 receptors

A
  1. CTLA-4 has a higher affinity for B7 than CD28 receptors -> decreased IL2 production
  2. CD28 is constitutively expressed while CTLA-4 is expressed a few days after T cell activation
  3. B7 bound to CD28 produces a positive signal while B7 bound to CTLA-4 produces a negative signal
49
Q

Similarities between CTLA-4 and CD28 receptors

A

Both are expressed on T cells
Both bind to B7 molecules

50
Q

What type of cell is PD-1 expressed in?

A

PD-1 is expressed in chronically activated T cells -> inhibits activation signals from TCR complex and CD28

51
Q

How do tumour cells evade T cell responses?

A
  1. Expression of PD-L1 on tumour cells -> binds to PD-1 on T cells -> inhibits activation signals from TCR complex and CD28
  2. Upregulation of CTLA-4 and PD-1 on tumour infiltrating lymphocytes -> inhibits T cell responses
  3. Recruitment of Treg -> constitutively expresses CTLA-4 -> inhibits T cell responses
52
Q

What is “checkpoint blockade”?

A

Antibodies that block CTLA-4 and PD-1 -> reduce inhibitory signals for T cells -> boost anti-tumour T cell responses -> tumour regression

53
Q

When there is a MMR deficiency in tumour, must use…

A

checkpoint blockade

54
Q

HIV-1 infects what type of cells?

A

CD4+ T cells

55
Q

At birth, the serum of newborns contain high levels of what?

A

Maternal IgG

56
Q

What is the half life of serum IgG?

A

3-4 weeks

57
Q

What is ESR and what does it measure?

A

ESR = erythrocyte sedimentation rate
It measures how fast erythrocytes settle to the bottom of the test tube. A faster than normal rate indicates inflammation.

58
Q

What is the Anti-Nuclear Antibiotics test?

A

Positive ANA test shows the presence of serum auto-antibodies that bind to components of cellular nuclei -> attack own cells
NOT a specific test for SLE

59
Q

What is the Anti-double stranded DNA test?

A

A specific test for SLE

60
Q

Pathophysiology of SLE

A

Pathological deposition of immune complexes within tissues -> triggers complement pathway activation

61
Q

What is complement pathway?

A

C3 is a complement that is broken down during complement activation by Fc receptors on antibodies
- smaller fragment: C3a = anaphylatoxin = pro-inflammatory mediator and recruits inflammatory cells
- larger fragment: C3b = opsonin = binds to cell surface to mark the cell for phagocytosis (but when the cell is too large for phagocytes to engulf, frustrated phagocytes will release lysomal enzymes extracellularly instead of intracellularly)

Decreased levels of C3, C4 = Increase disease activity due to the breakdown of complements that will release anaphylatoxins
=> disease activity monitored by INTACT serum C3, C4 levels

62
Q

What is the most common solid organ transplant?

A

Renal transplantation

63
Q

Complications of renal transplantation

A
  1. graft rejection
    - hyperacute rejection
    - acute rejection
    - chronic rejection
  2. infection
  3. relapse of disease
64
Q

Hyperacute Rejection

A
  • occurs within minutes of transplantation
  • mediated by pre-formed anti-donor antibiotics in the recipient (binds to donor antigens)
    -> complement dependent cytotoxicity
    -> opsonisation (phagocytes)
    -> ADCC (NK cells)

-> damage endothelium
-> vascular thrombosis
-> ischaemic necrosis of graft

65
Q

Acute Rejection

A
  • occurs days or weeks after transplantation
  • mediated by alloreactive recipient CD8 T cells -> kill transplanted allogenic graft cells that are recognised as foreign -> graft rejection
66
Q

Haematopoietic Stem Cell Transplantation

A

Use of CD34+ haematopoietic stem cells
- multipotent
- self-renewing

67
Q

Host versus Graft T cell response

A

residual alloreactive recipient CD8+ T cell reject donor’s HSC -> graft rejection

68
Q

Host versus Graft Antibody Response

A

preformed anti-donor antibodies in the recipient
–> complement dependent cytotoxicity
-> opsonisation (phagocytes)
-> ADCC (NK cells)
=> graft rejection

69
Q

Clinical manifestations of GvHD (graft versus host disease)

A

Acute GvHD - occurs within first 100 days of transplant
Chronic GvHD - occurs after 100 days

70
Q

Acute GvHD

A

alloreactive donor CD8+ T cells damage and kill recipient’s T cells
- priming phase
- effector phase

71
Q

What does adjuvant do?

A

Stimulates an innate immune response to augment adaptive immunity

72
Q

What are 2 types of adjuvants?

A

Emulsions and Mineral salts

73
Q

For what type of vaccines do we need adjuvants?

A

Purified components

74
Q

What are the 4 types of vaccines?

A
  1. Live attenuated vaccines
  2. Killed pathogens
  3. Toxoids
  4. Purified components
75
Q

What are the 4 phases of primary antibody response to antigen?

A

Lag, log, plateau, decline

CA1 Extra Qns (5 decks)

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