Immunology Flashcards
HLA B27 associated with PAIR
psoriasis
Ank spond
IBD
Reiters
Effect of IFN gamma on macrophages
Th1nk Big Mac attack
Th1 and NK cells Build IFN gamma
Augments macrophage ability to attack
Sjogrens features
MAPLES
mouth dry Arthritis Parotid enlargement Lymphoma Eyes dry Sicca (primary) or secondary
Digeorge syndrome disease of Ts
Third and fourth pharyngeal pouches absent
Twenty two chromosome
T cells absent
Tetany from hypocalcaemia (no PTH)
IL1
Produced my macrophages monocytes and dendritic cells
Activates T cells
B cells mature
Reset hypothalamus with il6, IFN, tnf
Il2
Thcells
Acts on T cells and NK cells - self activation
iL2 plus 4 leads to persistent IgM and not class switch
IL4
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
IL5
Growth and diff eosinophils
Produced by Th2
IL6
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
IL8
Chemokine . Attracts neuts
Macros and endothelial secrete when stimulated by IL1, TNF alpha, bacterial products so that can attract neuts
IL10
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
IL12
Major CK secreted by APCs to activate T cells and drive them down the Th1 pathway
Opposes effects Il4 on APCs
IFN Gamma
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
TNF alpha
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
TGF beta
Transforming growth factor
Secreted by plt macro lympho
Class switch to IgA
Attract macro and mono
Downregulate a macro and Excess T cell function
IL 13
Similar to IL4
IFN alpha
Antiviral activity
Expression MHC 1
Activate NK
IFN beta
Antiviral
Increase MHC 1 expression
Activate NK
What is the trigger for chronic urticaria and angioedema?
High dose antihistamines
AVOID STEROIDS oral/systemic
B cell surface markers? How do they change as time goes on??
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)
Which surface Igs to B cells have at different stages?
sIgM on Immature B cell
then
sIgM and IgD on naive B cell
In general terms, how do you treat cellular rejection vs antibody mediated rejection?
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
What is the Banff classification?
International classification of renal transplant pathology, but can be used for other organs.
- normal
- antibody mediated (classically stain positive for C4d but not always)
- borderline changes suspicious for T cell mediated rejection
- acute T cell mediated rejection
- interstitial fibrosis and tubular atrophy
- Other changes not due to rejection
Name some causes of long term renal allograft loss. (4)
Chronic allograft nephropathy from CNI toxicity, rejection
Death with functioning graft (CVD, malig)
Recurrent disease
BK nephropathy
How does bortezomib work?
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
How does campath work? (Alemtuzumab)
Anti CD 52
Depletes T cells profoundly
Induction therapy and immunosupression minimisation
T cells then repopulate ?T regs
How does Eculizumab work?
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
Anaemia of chronic disease - WHICH CYTOKINES ARE RESPONSIBLE?
IL-1 IL-6 TNF alpha.
Also IFN beta and IFN gamma
Best screening tool for hereditary angioedema? (low levels of C1-INH protein)
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
What is Rheumatoid factor, physically?
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%
What do TLR do?
proteins of the innate immune system
span membrane on dendritic and macrophages
recognise structurally conserved microbe molecules
activate innate immune response
Advantages of killed vaccines
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
IgA1 and 2 differ how
in their heavy chains
IgA1 in airways and serum
IgA2 in colon
How do you define a NK cell in CD ?
lack CD3
have CD56
FcRIII AKA CD16 is their receptor that binds the Fc portion of the Ab for ADCC
When do you do skin prick testing for venom?
if anaphylaxis
not if just large local reaction and no systemic symptoms
if negative, repeat several weeks later
How does immunotherapy work?
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
Who gets flu and pneumovax
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
If tryptase is up, why do you have to do a follow up sample when well
check for mastocytosis- atypical mast cells collect in liver and spleen and all over the place
SKIN TESTING IS FOR WHEN YOU THINK IT IS IgE MEDIATED!! NOT TYPE 2,3,4!!!!
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