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Immunology > Immunology > Flashcards

Immunology Flashcards

0
Q

HLA B27 associated with PAIR

A

psoriasis
Ank spond
IBD
Reiters

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1
Q

Effect of IFN gamma on macrophages

Th1nk Big Mac attack

A

Th1 and NK cells Build IFN gamma

Augments macrophage ability to attack

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2
Q

Sjogrens features

MAPLES

A 
mouth dry
Arthritis
Parotid enlargement
Lymphoma
Eyes dry
Sicca (primary) or secondary
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3
Q

Digeorge syndrome disease of Ts

A

Third and fourth pharyngeal pouches absent
Twenty two chromosome
T cells absent
Tetany from hypocalcaemia (no PTH)

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4
Q

IL1

A

Produced my macrophages monocytes and dendritic cells
Activates T cells
B cells mature
Reset hypothalamus with il6, IFN, tnf

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5
Q

Il2

A

Thcells
Acts on T cells and NK cells - self activation
iL2 plus 4 leads to persistent IgM and not class switch

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6
Q

IL4

A

Produced by Th2 and basophils
Promotes TH2 differentiation
Acts on active B cells–> increase proliferation
Tells to become a plasma cell and produce IgE- isotope switching
Eosinophil and mast cell growth and function
Immunoregulstes to decrease macro activity

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7
Q

IL5

A

Growth and diff eosinophils

Produced by Th2

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8
Q

IL6

A

Th2 is major source. Also mono macro and BM cells
Promote plasma cell differentiation
Hepatocyte stimulating factor - stimulates to make acute phase reactants
Induces fever

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9
Q

IL8

A

Chemokine . Attracts neuts

Macros and endothelial secrete when stimulated by IL1, TNF alpha, bacterial products so that can attract neuts

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10
Q

IL10

A

Important inhibitory role
Acts on macrophages to inhibit ck production to downregulate Th1 type of THC

RELEASD by Th2

Downregulates MHC2 on APC

With IL4 decreases macro activity

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11
Q

IL12

A

Major CK secreted by APCs to activate T cells and drive them down the Th1 pathway

Opposes effects Il4 on APCs

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12
Q

IFN Gamma

A

Secreted by NK and Th1 and cytotoxic T cells
Angers macs
Increase MHC I , increase antigen presentation
Increase MHC 2 expression on APCs
Class switch to IgG
Down regulatory effect on TH2 function
Induces IL12 production by macrophages which inhibits tH2
IFN AND TNF mediate TB inflamm
If deficiency of IFN OR ITS RECEPTOR prone to overwhelming mycobacterial infection

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13
Q

TNF alpha

A

Macrophages produce in response to gram negative and other microbial infections
Binds tumour cells and activates CAPSASE pathway–> death by apoptosis
Induces fever
Recruits cells to inflammation site
Potentiated by IFN gamma
Overproduction can lead to inflammation like arthritis or septic shock
Stimulates liver to produce acute phase proteins

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14
Q

TGF beta

Transforming growth factor

A

Secreted by plt macro lympho
Class switch to IgA
Attract macro and mono
Downregulate a macro and Excess T cell function

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15
Q

IL 13

A

Similar to IL4

16
Q

IFN alpha

A

Antiviral activity
Expression MHC 1
Activate NK

17
Q

IFN beta

A

Antiviral
Increase MHC 1 expression
Activate NK

18
Q

What is the trigger for chronic urticaria and angioedema?

A

High dose antihistamines

AVOID STEROIDS oral/systemic

19
Q

B cell surface markers? How do they change as time goes on??

A

CD 19 from pre-B cell to plasmablast (the one right before a mature plasma cell)
CD 20 from Pre-B cell right through to plasmablast- NOT memory or plasma B cells
CD40 from Activated B cell to Plasma cell (CD40 is the most important for interaction between B and T cells that activate the B cells)

20
Q

Which surface Igs to B cells have at different stages?

A

sIgM on Immature B cell
then
sIgM and IgD on naive B cell

21
Q

In general terms, how do you treat cellular rejection vs antibody mediated rejection?

A

Cellular: Signal 1 with cyclosporine A, Tac, Signal 2 with CTLA4 Ig (belatacept)- binds B7, Signal 3 with anti CD 35 and MTOR inhibs, “late” blockers with MMF and AZA, and depletion with ATG

Antibody: plasma exchange, andti CD20 which is ritux, and proteasome inhibitors

22
Q

What is the Banff classification?

A

International classification of renal transplant pathology, but can be used for other organs.

  1. normal
  2. antibody mediated (classically stain positive for C4d but not always)
  3. borderline changes suspicious for T cell mediated rejection
  4. acute T cell mediated rejection
  5. interstitial fibrosis and tubular atrophy
  6. Other changes not due to rejection
23
Q

Name some causes of long term renal allograft loss. (4)

A

Chronic allograft nephropathy from CNI toxicity, rejection
Death with functioning graft (CVD, malig)
Recurrent disease
BK nephropathy

24
Q

How does bortezomib work?

A

Proteosome inhibitor

NFkB is critical for memory B cells and plasma cells.
IkB inhibits NFkB but is kept in check by proteosomes which degrade IkB.
Proteosome inhibitor blocks IkB degradation–>heaps of IkB to inhibit NFkB

25
Q

How does campath work? (Alemtuzumab)

A

Anti CD 52
Depletes T cells profoundly
Induction therapy and immunosupression minimisation
T cells then repopulate ?T regs

26
Q

How does Eculizumab work?

A

C5a complement inhibitor

When anti-HLA Ab bind, they cause complement activation–>MAC
Eculizumab binds C5 with high affinity and prevents cleavage to C5a and b and hence formation of the MAC

27
Q

Anaemia of chronic disease - WHICH CYTOKINES ARE RESPONSIBLE?

A

IL-1 IL-6 TNF alpha.

Also IFN beta and IFN gamma

28
Q

Best screening tool for hereditary angioedema? (low levels of C1-INH protein)

A

Serum C4 is the most reliably low inbetween attacks
C2 also low

C1-INH low during attack

Treatment is acutely IV C1 inhibitor concentrate, FFP if this is not available
Prophylaxis: anabolic steroid Danazol may help

29
Q

What is Rheumatoid factor, physically?

A

An IgM molecule reacting against the patients own IgG

Sjogrens and Feltys see about 100%
IE 50%
SLE 20-30%
RA 70%
Gen pop 5%
Systemic sclerosis 30%
30
Q

What do TLR do?

A

proteins of the innate immune system
span membrane on dendritic and macrophages
recognise structurally conserved microbe molecules
activate innate immune response

31
Q

Advantages of killed vaccines

A

non virulent
heat stable
less likely contaminated

live though are good in that can give via natural route and induce an A and G response, stronger and longer protection, virus can multiply in host and cause CD8 response

32
Q

IgA1 and 2 differ how

A

in their heavy chains
IgA1 in airways and serum
IgA2 in colon

33
Q

How do you define a NK cell in CD ?

A

lack CD3
have CD56

FcRIII AKA CD16 is their receptor that binds the Fc portion of the Ab for ADCC

34
Q

When do you do skin prick testing for venom?

A

if anaphylaxis
not if just large local reaction and no systemic symptoms

if negative, repeat several weeks later

35
Q

How does immunotherapy work?

A

Alters T cell reactivity to certain Ag which causes reduction in release of pro-allergic/inflammatory cytokines

cant do for food
new evidence that it is not the blocking ab so much

36
Q

Who gets flu and pneumovax

A

Flu- ATSI over 50, caucasian over 65
Pneumococcal- same

Pneumococcal

  • splenectomy
  • sickle cell over 2 years old
  • chronic resp, heart, renal disease
  • CSF leak
  • HIV, lymphoma, myeloma, nephrotic syndrome
37
Q

If tryptase is up, why do you have to do a follow up sample when well

A

check for mastocytosis- atypical mast cells collect in liver and spleen and all over the place

38
Q

SKIN TESTING IS FOR WHEN YOU THINK IT IS IgE MEDIATED!! NOT TYPE 2,3,4!!!!

A

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Immunology (16 decks)

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