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immunology > the basics > Flashcards

the basics Flashcards

1
Q

broadly - what is the difference between the innate and adaptive immune response?

A

innate - non-specific, immediate but has no memory and will act in the same way each time

adaptive - specific and diverse, has a memory, but must be primed and takes days-weeks to peak

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2
Q

which are the APCs

A

monocytes
macrophages
dendritic cells

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3
Q

which are the phagocytic cells

A

neutrophils
monocytes
macrophages
dendritic cells

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4
Q

where are mature B and T cells made

A

mature B in spleen
mature T in thymus

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5
Q

T cell development in thymus up to DP stage

A

common lymphoid progenitor first at DN1 stage = double neg (CD3-, CD4-, CD8-)
- thymus epithelial cells express IL2 and IL7
- these stimulate enzymes RAG1 and RAG2 (=VDJ recombinase) - now at DN2 stage
- successful D and J segment joining - now DN3
- VDJ joined with constant region to form beta chain- now DN4

  • beta chain + practice alpha chain + CD3 all expressed > produces daugther cells with CD4 and CD8 - now DP stage
  • rearranges practice alpha to make distinct TCR
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6
Q

T cell development in thymus post DP stage

A

positive selection: can the TCR recognise the person’s own MHC? –> the ones that do keep going on

then negative selection: AIRE allows thymic epithelium to express self-antigens. If the DP cell joins strongly, it will die.

SP naive T cell will downregulate CD8 if binds strongly to MHCII to become a CD4 naive T cell. if binds weakly -> CD8 T cell.

… then goes to secondary lymphoid tissue

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7
Q

T cell receptor vs B cell receptor chains

A

T cell = alpha (VJ) and beta (VDJ) (think, white people alpha, no diversity)

B cell = light chain like alpha, heavy like beta

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8
Q

complete RAG1/RAG2 deficiency causes what

A

SCID!

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9
Q

CD4 vs CD8 T cells

A

CD4 = helper cells (the FBI) - recognise antigen on MHCII
CD4 = cytotoxic T cells (SWAT team!). recognise antigen on MHCI

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10
Q

MHCI vs MHCII

A

MHCI: encode HLA proteins with one letter (hla-a/b/c)
- on all nucleated cells, even platelets!
- present endogenous peptides
- activate CD8 T cells

MHCII: encode HLA proteins with two letters (hla-dp/dq/dr)
- on APCs only
- present extracellular peptides
- activate CD4 T cells

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11
Q

Th1 vs Th2 vs Th17 fight what kinds of infection?

A

Th1 = intracellular infection
Th2 = parasites
Th17 = fungal and bacterial infections

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12
Q

Th1 vs Th2 vs Th17:
- how do they develop from Th0
- cytokine profile

A

Th1:
- development: IL-12 (from APC), IFN-gamma (from Th1 itself)
- makes: IL-2 (T cell proliferation), IFN-gamma (activates macrophages), TNF-alpha, IL-12 (positive FB)

Th2:
- development: IL-4 (from NK and from self)
- makes: IL-4, IL-5, IL-13

Th17:
- develop: TGF-beta, IL-6, IL-21, IL-23
- makes: IL-17 (and IL-6 and TNF-alpha)

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13
Q

where do these cytokines come from:
IL-12
IFN-gamma
IFN alpha
IFN beta

A

IL-12: macrophages and dendritic cells
IFN gamma: NK cells
IFN alpha: viral infected cell
IFN beta: viral infected cell

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14
Q

condition from no Th17 cells?

A

Autosomal dominant hyperIgE syndrome (STAT3) - susceptible to fungal infections!

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15
Q

what do T reg cells do?

A

suppress immune response via TGF-beta and IL-10
needs FoxP3 transcription factor to work and develop

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16
Q

deficiency of Treg FoxP3 results in what?

A

IPEX!

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17
Q

IL-10 deficiency or defects cause what?

A

early onset IBD!

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18
Q

uncontrolled Th1 vs Th2 vs Th17 responses are associated with what problems?

A

Th1 –> autoimmunity
Th2 –> allergy/asthma
Th17 –> also autoimmunity

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19
Q

predominant roles of:
IL-2
IL-4
IL-5
IL-10
IL-12
IFN-gamma
TGF - beta

A

IL-2 = T cell expansion
IL-4 = B cell switch to IgE
IL-5 = activate eosinophils
IL-10 = immune regulator (anti-inflammatory)
IL-12 = Th1 differentiation
IFN-gamma = activate macrophages
TGF-beta = anti-inflammatory

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20
Q

describe b cell development- antigen independent

A

in bone marrow
common lymphoid progenitor undergoes:
- heavy chain D-J combo, then VDJ combo
- then heavy VDJ joins constant mu region for IgM
- paired with surrogate light chain, if successful, cell proliferates
- then light chain VJ combo - first with kappa, then lambda chain genes
- if NOT-REACTIVE, will express IgD constant region to be released into periphery as immature B cell

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21
Q

plasma vs memory B cell

A

Plasma cell = produce large amounts of Ab of particular antigen specificity
Memory B cell = long-lasting cells able to rapidly produce high-affinity antibodies in response to second antigen challenge

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22
Q

T cell dependent vs independent b cell activation

A

independent:
- polysaccharide antigens usually
- only IgM
- short lived plasma cells, but rapid response

dependent:
- occurs at interface of primary follicle (B) and parafollicular cortex (T)
- Ag causes crosslinking of BCR > Ag internalised
- Ag presented on B cell to CD4 Th using CD40-CD40L (ligand on Th)
- this induces isotype switching in B cell, depending on cytokine mlieu

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23
Q

which cytokines cause which isotype switch?

A
  1. IL-10 > IgG1/3
  2. IL-4/IL-13 > IgE
  3. TGF-beta > IgA
24
Q

valence = what?

A

number of fab regions!

25
Q

order of Ig in terms of time, and % of Ig population

A

IgM (D) (5%) > IgG (75%) > IgA (20%) > IgE (<1%)

26
Q

major roles of the different Igs

A

IgM: activates complement
IgD: helps B cells leave bone marrow
IgG: opsonisation, and activate classical complement pathway, and ADCC
IgA: opsonisation, main Ig in mucosa
IgE: allergic and anti-parasitic responses

27
Q

which is the only Ig type to cross the placenta

A

IgG

28
Q

at what age do Ab deficiencies often present, and why?

A

nadir of IgM at 3-6months due to passive immunity from mum running out and own kicking in slowly

29
Q

parts of an Ig

A

Fab = antigen binding site
Fc = Fc receptor binding / complement binding site

30
Q

which kind of Ig is not lost in a protein losing enteropathy and why?

A

IgM - because its so large as a pentamer!

31
Q

when do IgM, IgG and IgA reach adult levels?

A

IgM 1yo
IgG 5yo
IgA adolescence

32
Q

MHCI and II deficiency leads to what conditions?

A

MHCI deficiency > bare lymphocyte syndrome (BLS) I
MHCII > BLSII

in both, defect is in the accessory transcriptors, not the MHC itself
like SCID

33
Q

which is the only APC that activates naïve T cells and initiate an immune response?

A

dendritic cell

34
Q

the three granulocyte cells are…

A

eosinophil, neutrophil, basophil

35
Q

what two enzymes to be aware of for neutrophil oxidative killing

A

MPO
NADPH oxidase

36
Q

complement made where?

A

liver!

37
Q

the three complement pathways are…?

A
  1. classical
  2. alternative (always at work tho)
  3. lectin binding pathway
38
Q

classical complement pathway

A

-Ag-Ab immune complex binds C1q
-activated C1 cleaves C4 and C2 –> C4b+C2b = C3 convertase
-cleaves C3 –> C3b is opsonin!
- C3b also binds C4bC2b –> C4bC2bC3b = C5 convertase
- cleaves C5 –> C5b binds C6,C7,C8, and along with C9 = MAC

39
Q

lectin binding pathway

A

mannose binding lectin protein binds mannose on pathogen
MBLP is similar shape to C1 - so from then on, is same as classical pathway

40
Q

alternative complement pathway

A

-C3 cleaved in absence of C3 convertase, so always some C3b hanging
-C3b binds Bb (from factor B) = this is also a C3 convertase! therefore this is an amplification step
- then same as classical pathway

41
Q

deficiency in C5 to C8 will make pt susceptible to what?

A

neisseria, gono, meningitis

42
Q

deficiency of C1 to C4 causes what kind of illness?

A

lupus-like

43
Q

C3a and C5a functions

A

chemotaxin (recruit cells to the site of inflammation) and anaphylotoxin (help cells degranulate)

C5a is also an opsonin with C3b!

44
Q

opsonins of the complement pathway

A

C3b and C5a

45
Q

what are 3 key inhibitors of the complement pathway, and deficiencies of each lead to what disease?

A

C1 esterase inhibitor -> hereditary angioedema
factor H and I -> atypical HUS

46
Q

phyiology of a fever

A

-Neutrophils/macros phagocytose bacteria and make pyrogen IL1
-IL1 goes to anterior hypothal –> PGE
-PGE raises the set point so you feel cold, and the body will inc temp by shivering, VC

47
Q

what stage of life is lymphocyte count highest

A

at birth and up to 2 y of life! so lymphopaenia when young is defo baddos

48
Q

what is a measure of thymic output?

A

naive T cell measurement = TREC, formed in the process of TCR rearrangement

49
Q

these CDs are a marker of what?
C45+
CD3+
CD3+/CD4+
CD3+/CD8+
CD19+ or CD20+
CD16+ and CD56+ and CD3-
CD27+

A

C45+ = pan-leukocyte
CD3+ = T cell
CD3+/CD4+ = helper
CD3+/CD8+ = cytotoxic
CD19+ or CD20+ = B cell
CD16+ and CD56+ and CD3- = NK cell
CD27+ = memory B cell

50
Q

Pneumovax 23 vs tetanus vax - what kind of B cell activation do they use?

A

Tetanus (T dependent B cell response) = protein + polysaccharide
Pneumovax 23 (T independent B cell response) = polysaccharide ONLY

51
Q

classical vs alternative complement pathways test

A

classical: CH50 or THC
Alternative pathway activity: AP50 assesses factor, D, B and properdin

52
Q

what kind of C3/C4 results suggest classical vs alternate complement pathway activation?

A
  • Both low – suggests classical pathway
  • Normal C4, low C3 – suggests the alternative pathway
53
Q

mast cell tryptase peaks and returns to baseline when?

A

peaks - 1-2 hours
returns to baseline - in 6 hours

54
Q

half lives of the Igs

A

IgD/E 3 days
IgM/A 6 days
IgG 24 days

55
Q

what will TREC test miss?

A

Omenn “leaky SCID”

immunology (3 decks)

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