Eosinophils/IgE - Type 2 vs Type 1 HS ?

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winsicle

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I had a ? on Qbank about what type of HS reaction in Ascaris infection. The answer was Type 1.

I thought that invasive worms induce a Type 2 HS (cytotoxic reaction) wherein the eosinophil's IgE receptors bind to the organisms "IgE-like" surface ligands --> releasing MBP, etc. killing the organism.

What am I missing here?

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So the key is that Type II = antibody stimulating complement (IgG and IgM are the ones that do this). The reaction you described with IgE is not complement mediated. You should get the mast cell degranulation and release of histamine with a hellminth infection (immediate hypersensitivity), but the infection is frequently asymptomatic becasue the hellminth doesn't invade tissue all that often (it just crawls around and sometimes plugs up your bile duct).
 
Hmm, looking at Goljan's RR (pg. 40/44-45) he describes IgE mediated type I AND II HS, so what's the deal here - is HE wrong or is QBank wrong?

and BTW he states the IgE-mediated type 2 reaction as Complement-independent
 
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you can have a type 2 using IgE-eosinophil killing (it doesn't need complement to make it a type 2...just an antibody to a cell).....but if the worm isn't "invasive" you won't get that mechanism and type 1 will predominate
 
Elevated Eosinophils= cancer, asthma,parasites,allergies.ect.

Also remember that

Type 1 the mast cells well degranulate, and you will have high IgE

Type 2 The cell will say Hey dude inside of me there is a :thumbdown:, so kill me before its spreads.

I hope this helps
 
Type 1 hsn rxn
NAACP---true
but...
Also remember that ONLY
INVASIVE HELMINTHS CAUSE INC IN EOSINOPHILS
eg:strongy and hookworm
NON INVASIVE...DONT INC EOSINOPHILS.
eg: pinworm and adult ascaris

***larvae of ascaris invade and cause an increase of eos but the adult forms dont incvade.*****

I had a ? on Qbank about what type of HS reaction in Ascaris infection. The answer was Type 1.

I thought that invasive worms induce a Type 2 HS (cytotoxic reaction) wherein the eosinophil's IgE receptors bind to the organisms "IgE-like" surface ligands --> releasing MBP, etc. killing the organism.

What am I missing here?
 
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