1 micro question...halp >_<

[lilmisty]

Can someone help me out?

How does the body deal with intracellular infections that AREN'T viruses? For example, Listeria (bacteria), Histoplasma capsulatum, and Plasmodium are all intracellular! Is it all just with cell-mediated immunity (aka macrophages)? Or are antibodies involved? Cd8? ?! AHHHH!

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[dyspareunia]

Can someone help me out?

How does the body deal with intracellular infections that AREN'T viruses? For example, Listeria (bacteria), Histoplasma capsulatum, and Plasmodium are all intracellular! Is it all just with cell-mediated immunity (aka macrophages)? Or are antibodies involved? Cd8? ?! AHHHH!

In short, granulomas.

 

[CherryRedDracul]

Can someone help me out?

How does the body deal with intracellular infections that AREN'T viruses? For example, Listeria (bacteria), Histoplasma capsulatum, and Plasmodium are all intracellular! Is it all just with cell-mediated immunity (aka macrophages)? Or are antibodies involved? Cd8? ?! AHHHH!

Cell-mediated. The IL-12/IFN-gamma axis is critical for immune responses against intracellular bacteria. After macrophages try to eat these critters up, they have a difficult time digesting them in their phagolysosomes because these bacteria have adaptations to survive against them. So, macrophages secrete IL-12 which activates NK or CD4+ T cells to release IFN-gamma, giving the macrophages extra firepower to digest the microbes. CD8+ T cells, on the other hand, "take care" of infected cells (R.I.P.).

Persistent infection with intracellular bacteria --> granulomatous inflammation, classically seen with M. tuberculosis.

 

[lilmisty]

Thanks you two (especially CherryRed!).

I'm assuming that once that Macrophages eat the bugs up, they can present to CD4 which will have two responses: probably have some crappy B cell response (via Th1) that is virtually useless (ain't no IgG getting those bugs) and then a Th2 response that does most of the work?

 

[CherryRedDracul]

Thanks you two (especially CherryRed!).

I'm assuming that once that Macrophages eat the bugs up, they can present to CD4 which will have two responses: probably have some crappy B cell response (via Th1) that is virtually useless (ain't no IgG getting those bugs) and then a Th2 response that does most of the work?

Actually, it would be Th1 that would be doing the majority of the killing work. IL-12 secretes by macrophages stimulates CD4+ helper T cells to become Th1 cells.

Th1: secretes IFN-gamma ---> activates macrophages and CD8+ cytotoxic T cells.
Th2: secretes IL-4, IL-5, IL-6, IL-10, IL-13 --> humoral response with B cells (IL-4 promotes class switching from IgM to IgG).

 

[lilmisty]

Right my bad! Also, do you think that in people who have diseases that result in T-cell dysfunction (ie, DiGeourge) would be predisposed to intracellular bacterial infections too? Or just the classic viral and fungal disease?