Notes 4.29

I. Immunopathology: Types of hypersensitivity reactions
a) Type I (anaphylactic type)
-IgE against common environmental antigen (harmless)
*allergies, asthma
*Hygiene hypothesis-allergies more prevalent in cleaner societies because
don’t have parasites; no target for IgE
b) Type II (cytotoxic type)
-You make IgG or IgM against own antigens, kill own cells with CD8+
T-cells (organ rejection)
>some prolonged bacterial infectionsantibodies against shared
bacterial/self epitopes (ex: Syphilis- T. pallidum bacteria share
lots of epitopes with human cells)
c) Type III (immune-complex type)
-Make IgG or IgM against own free antigens (not bound to cell surface)
-Clots of antibody and antigen can block very small vessels-blockage
symptoms (ex: lupus)
d) Type IV (cell-mediated type)
-Delayed, takes ~48 hrs after exposure to have reaction
-This is because reaction is against antigen from intracellular pathogen
that’s had its antigens presented to T-cells by APCs (in past)
>If re-exposed, CD8+ T-memory cells recruited to site of
re-exposure
i. the PPD test, and why we don’t vaccinate for tuberculosis in the USA
-TB rate low and we have antibiotics that work against TB
*If we vaccinated, PPD test wouldn’t accurately ID TB carriers
-Reverse of herd immunity, lots of TB-carriers so vaccine makes
more sense.

PPD Test
-TB antigens injected under skin, checked 48-72 hrs later
-TB vaccine: inject live vaccine, related to TB-bacteria
>CD8+ T-memory cells against vaccine bacteria
*Not a lot of good TCR antigens on TB or vaccine bacteria cell
wall
so, T-memory cells response weak
-TB stops phagolysosome formation
>survives in macrophages very well
>hard to make TCRs, antibodies against
will always have forever

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