1 micro question...halp >_<

[lilmisty]

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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!

 

[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?