why di george doesn't have bacterial susceptibility as well?

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jfgavina

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since Th2 cells are very important to stimulate b-cell class switching and stimulation?

sorry for the title, read "hasn't" instead of doesn't have of course
 
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since Th2 cells are very important to stimulate b-cell class switching and stimulation?

sorry for the title, read "hasn't" instead of doesn't have of course

it does. but you can still make lots of IgM and some IgG even if you can't make Th2 cells. the bigger issue is the T-cell problem, and that if the patient has a bacterial problem, it's related to lack of T-cell dependent B-cell activation.
 
since Th2 cells are very important to stimulate b-cell class switching and stimulation?

sorry for the title, read "hasn't" instead of doesn't have of course


have you heard of T-cell independent B-cell activation?

repeated antigens on bacteria such as LPS can bind to several B-cell receptors on one B-cell and cluster these B-cell receptors. clustering of these receptor lead to B-cell activation.
This obviously does not apply to all bacteria.


Also for completion, there is T-cell independent polyclonal B-cell activation which occurs when antigens on parasites bind to certain proteins on B-cell (different from B-cell receptors) which are linked with B-cell receptors. clustering of those proteins lead to clustering of B-cell receptors and you get a polyclonal activation.
The former is antigen specific activation the latter is not.
 
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