the basics Flashcards by Grace W

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

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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which are the APCs

monocytes
macrophages
dendritic cells

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which are the phagocytic cells

neutrophils
monocytes
macrophages
dendritic cells

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where are mature B and T cells made

mature B in spleen
mature T in thymus

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T cell development in thymus up to DP stage

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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T cell development in thymus post DP stage

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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T cell receptor vs B cell receptor chains

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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complete RAG1/RAG2 deficiency causes what

SCID!

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CD4 vs CD8 T cells

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

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MHCI vs MHCII

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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Th1 vs Th2 vs Th17 fight what kinds of infection?

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

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

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

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

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condition from no Th17 cells?

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

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what do T reg cells do?

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

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deficiency of Treg FoxP3 results in what?

IPEX!

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IL-10 deficiency or defects cause what?

early onset IBD!

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

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

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

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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describe b cell development- antigen independent

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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plasma vs memory B cell

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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T cell dependent vs independent b cell activation

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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which cytokines cause which isotype switch?

Study These Flashcards

IL-10 > IgG1/3
IL-4/IL-13 > IgE
TGF-beta > IgA

valence = what?

Study These Flashcards

number of fab regions!

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

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

major roles of the different Igs

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

which is the only Ig type to cross the placenta

IgG

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

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

parts of an Ig

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

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

IgM - because its so large as a pentamer!

when do IgM, IgG and IgA reach adult levels?

IgM 1yo IgG 5yo IgA adolescence

MHCI and II deficiency leads to what conditions?

MHCI deficiency > bare lymphocyte syndrome (BLS) I MHCII > BLSII in both, defect is in the accessory transcriptors, not the MHC itself like SCID

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

dendritic cell

the three granulocyte cells are...

eosinophil, neutrophil, basophil

what two enzymes to be aware of for neutrophil oxidative killing

MPO NADPH oxidase

complement made where?

liver!

the three complement pathways are...?

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

classical complement pathway

-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

lectin binding pathway

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

alternative complement pathway

-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

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

neisseria, gono, meningitis

deficiency of C1 to C4 causes what kind of illness?

lupus-like

C3a and C5a functions

chemotaxin (recruit cells to the site of inflammation) and anaphylotoxin (help cells degranulate) C5a is also an opsonin with C3b!

opsonins of the complement pathway

C3b and C5a

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

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

phyiology of a fever

-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

what stage of life is lymphocyte count highest

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

what is a measure of thymic output?

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

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

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

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

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

classical vs alternative complement pathways test

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

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

- Both low – suggests classical pathway - Normal C4, low C3 – suggests the alternative pathway

mast cell tryptase peaks and returns to baseline when?

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

half lives of the Igs

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

what will TREC test miss?

Omenn "leaky SCID"

the basics Flashcards

(55 cards)