Immuno - E4 review slides Flashcards
What are the functions of complement
Opsonization requires C3b
Chemotaxis requires C3a and C5a
Anaphylatoxin requires C3a and C5a
Cytolytic activity requires the MAC components (C5b-C9)
Cytokines From Antigen presenting cells
IL-1 TNF IL-6 IL-12 Chemokines IL-10 - Inhibitory
Cytokines From Th1 cells
IFN-gamma
IL-2
Cytokines from Th2 cells
IL-4
IL-5
IL-13
Cytokines from CD17 cells
IL-17
Cytokines from Treg
IL-10
TGF-beta
CD Proteins
B-cells CD19, CD20
T-cells CD3, CD4 or CD8, CD28
Treg-cells CD4, CD25
Human MHC
MHC - an area on short arm (p) of chromosome 6. On short arm there is the HLA region –> codes for genes that make antigen and are crucial for transplantation. (whole thing: “haplotype”)
Class I molecule (A, B, C) - expressed only on APCS, binds CD4+
Class II molecule (DP, DQ, DR) - expressed on all nucleated cells, binds CD8+
Hyperacute rejection
to pre-formed antibodies in the recipient against the donor. Takes minutes or hours
Acute Rejection
due mainly to CMI (both CD4 and CD8 cells) against donor MHC molecules. Also some antibody attack. Takes 10-14 day
Chronic rejection
due to CMI and antibody attack
GVD
rxn of DONOR T cells against RECIPIENT MHC
CD4 in graft are activated
CD8 killing mechanism
CD8 molecule binds to MHC Class l (presenting tumor antigen)
T cell releases granzymes and perforins and the Fas-Fas L interaction
CD8=principle defense against
Virus infected cells
Intracellular bacteria (like TB)
Fungi
Tumors
NK cells
not T-cells (no T-cell receptors), nor B-cells ( no immunoglobulin receptors)
large granular lymphocytes (LGL’s)
Rec cells that lost Class I MHC and kill (similar mech to CD8--> use granzymes and perforin) OR ADCC (bind to IgG
Late phase of the acute allergic reaction
eosinophils, neutrophils, T-cells and mononuclear cells migrate to area –> release proinflammatory cytokines
Bird-fanciers
inhales antigen –> makes IgG
Next time she inhales –> antigen binds complement etc.
Also has T cells activated
*both type III & type IV
Contact dermatitis
T-cell mediated so the cells at the site of the inflammation would be macrophages, dendritic cells, CD4+ and CD8+ T-cells. You will not find antibody, complement or B-cells
Candida
Type IV hypersensitivity
His serum IgA, IgG and IgM levels are markedly decreased. –> SCID
candidiasis (thrush) –> Type IV
Both –>
SCID
GVD tx and prevention
Tx: Immunosuppression with drugs such as cyclosporine
To prevent GVD: Try to remove all the T-cells from the donor bone marrow preparation.
( In practise this is almost impossible to do)
Wiskott-Aldritch Syndrome
thrombocytopenia
eczema
recurrent infections
HIV sx
Delayed hypersensitivity skin tests to Candida or other antigens will be absent
The ratio of his CD4:CD8 cells will be reversed
B-cells will be normal
His blood will have antibodies to HIV (bc he has B-cells)
IgG levels will be normal or raised
He may now have trouble producing antibodies against new antigens because of the lack of T-cell help e.g. flu vaccine
Which of the following patients would not have increased susceptibility to infection with Mycobacterium tuberculosis?
A) Patient with a mutation of the IL-2 receptor
B) Patient with a mutation of the IL-12 receptor
C) Patient with a mutation of the RAG-1 gene
D) Patient with a mutation of the CD 28 gene
E) Patient with a mutation of the Btk gene
E (T cell not blocked)
Defective Btk, Bruton’s Tyrosine Kinase; necessary for maturation of pre-B-cells)
-NO MATURE B-CELLS.
