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Immunology 3 - Cellular immune response (ii) (Clinical assessment of T…
Immunology 3 - Cellular immune response (ii)
Superantigens
bind outside HLA group, but part of TCR-complex
well-conserved, activate large portions of T cell repertoire
cause massive ck surge + overwhelms Tregs (! sepsis)
can be viral or bacterial (e.g. TSST1, staphylococcal enterotoxin)
Th Subtypes
based on ck production profile
Th1
activates macrophages (via IFNgamma - R on macrophage - + CD40L - CD40 on macrophage, can remove TB) + Tc cells
cellular response against intracellular pathogens
granuloma formation (requires Th1, macrophages that sometimes become multinucleate giant cells, TFNgamma, TNFalpha)
Th2
activates B cells
humoral response
esp useful for IgE switching (NB helminths)
Th17
produces IL17,21,22
activate fibroblasts, epithelial cells + neutrophils
against intracellular pathogens
Tregs
downreg Th
How Tcs kill target cells
interaction via adhesion molecules (e.g. LFA1)
if antigen-specific reaction occurs, stable pairing + focused release of effector molecules
target cell dies, Tc released and moves on
1st response to a pathogen = innate
post-vaccine response = neutralising Igs
blocks a virus binding to host cells
How viruses enter host cells
bind to cell surface R
R-mediated endocytosis
acidification of endosome - virus + cell fuse
entry of viral DNA
Clinical assessment of T cell function
Hx (infections + vaccine problems)
HIV HX + test
WCC
should be x3 higher in children (DRs forget this and hence paed leucopenia often missed)
detailed (T cell nos + subtypes, expression of TCRs + CK Rs)
delayed hypersensitivity skin tests
prolif assays
vaccinate with protein antigens
reasons for poor T cell function
SCID
post-transplant
drug-induced
live attenuated vaccines
BCG
rotavirus
MMR