Immuno question from NMBE 4 ??

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

nope80

Resident
15+ Year Member
Joined
Apr 10, 2004
Messages
1,094
Reaction score
6
There was a question on NBME 4 I was hoping someone could help me out with: it was a woman w a 10 hour history of fever, chills, abdominal pain that radiated to right shoulder blade. History of gall bladder disease. High fever, abdominal pain with guarding, etc etc. Wanted to know which cytokines were involved in the patients condition???

Options were interferon gamma, IL4, IL10, TGF-b, tumor necrosis factor alpha

Any ideas??

Members don't see this ad.
 
Also, along the same lines, there was another immuno question about cytokines involved in septic shock? There were like 8 answer choices - I think it said the answer was tumor necrosis factor. I was always under the impression that there were a whole host of acute phase reactant thats contributed to this. For the sake of the test, can we just assume tumor necrosis factor as the culprit?
 
There was a question on NBME 4 I was hoping someone could help me out with: it was a woman w a 10 hour history of fever, chills, abdominal pain that radiated to right shoulder blade. History of gall bladder disease. High fever, abdominal pain with guarding, etc etc. Wanted to know which cytokines were involved in the patients condition???

Options were interferon gamma, IL4, IL10, TGF-b, tumor necrosis factor alpha

Any ideas??

I'm gonna go with TNF-Alpha.

We know it's not IL-4 because that's involved in isotype switching to IgE.

We know it's not IL10 because that supresses T cells.

We know it's not TGF-beta because that is more immunosuppressive.

Now between TNF-Alpha and IFN-Gamma... I know TNF-Alpha stimulates acute phase reactants (involved in this situation) and fever (in question stem). 50/50 shot and I'd choose TNF-Alpha.
 
Also, along the same lines, there was another immuno question about cytokines involved in septic shock? There were like 8 answer choices - I think it said the answer was tumor necrosis factor. I was always under the impression that there were a whole host of acute phase reactant thats contributed to this. For the sake of the test, can we just assume tumor necrosis factor as the culprit?

TNF-Alpha stimlulates acute phase reactant production/release.
 
Members don't see this ad :)
Another - man with chronic cough and night sweats. Transbronchial biopsy shows nodules with histiocytes and multinucleated giant cells. What is responsible for this?
Fibroblast growth factor on fibroblasts
IFNg on macrophages
IL1 on macrophages
IL1 on t lymph
IL2 on t lymph
Platelet derived growth factor on fibroblasts


No clue???!
 
FA2009 on page 201

I would say IL-2 because it increases T-cell proliferation

Granulomas are made up of epithelioid cells and giants cells (derivatives of macrophages) and also TH1 cells and fibroblasts
 
Another - man with chronic cough and night sweats. Transbronchial biopsy shows nodules with histiocytes and multinucleated giant cells. What is responsible for this?
Fibroblast growth factor on fibroblasts
IFNg on macrophages
IL1 on macrophages
IL1 on t lymph
IL2 on t lymph
Platelet derived growth factor on fibroblasts


No clue???!



edit: I found what I wrote down exactly:
Th1 cells (cell mediated immunity) secretes IL2 and IFNg. IL2 stimulates autocrine prolif of Th1. IFNg activates mphages promoting granuloma formation.
 
Last edited:
Th1 cells secrete Il-2 which activate proliferation of Th1 cells and also cytotoxic t-cells, right? Just want to make sure I have all the pathways right...
 
Another - man with chronic cough and night sweats. Transbronchial biopsy shows nodules with histiocytes and multinucleated giant cells. What is responsible for this?
Fibroblast growth factor on fibroblasts
IFNg on macrophages
IL1 on macrophages
IL1 on t lymph
IL2 on t lymph
Platelet derived growth factor on fibroblasts


No clue???!

I would go with INF gamma. It sounds like the option is saying INF gamma acts on macrophages, not produced by them. And multinucleated giant cells are macrophages. It goes monocytes > macrophages > epitheliod cells > multinucleated giant cells. The IL-2 will induce T lymphocytes, but it isn't a specific inducer for the Th1 subset of CD4 + T-cells, which produce the INF gamma...therefore, INF gamma acting on macrophages is more directly responsible for multinucleated cell formation.
 
I would go with INF gamma. It sounds like the option is saying INF gamma acts on macrophages, not produced by them. And multinucleated giant cells are macrophages. It goes monocytes > macrophages > epitheliod cells > multinucleated giant cells. The IL-2 will induce T lymphocytes, but it isn't a specific inducer for the Th1 subset of CD4 + T-cells, which produce the INF gamma...therefore, INF gamma acting on macrophages is more directly responsible for multinucleated cell formation.

:thumbup:

The key is that the question is describing a granuloma, and a granuloma cannot form without macrophage activation. IFNg produced by Th cells is the #1 cytokine responsible for macrophage activation. My memory is telling me that IFNg can also directly cause epithelioid cells (activated macrophages) to fuse into giant cells. Don't know if it directly does or not, but it is definitely a consequence of activation in the context of the question.
 
:thumbup:

The key is that the question is describing a granuloma, and a granuloma cannot form without macrophage activation. IFNg produced by Th cells is the #1 cytokine responsible for macrophage activation. My memory is telling me that IFNg can also directly cause epithelioid cells (activated macrophages) to fuse into giant cells. Don't know if it directly does or not, but it is definitely a consequence of activation in the context of the question.

Yes. Th1 cells secrete IFN-gamma to activate the macrophages and allow them to kill the intracellular MTB bacteria. Someone with Jobs syndrome (Now called Hyper-IgE Syndrome) has a deficiency of IFN-gamma and therefore chemotaxis is messed up because that wing of the adaptive response is gone (so a staph abscess will be "cold" rather than hot because the lack of chemotaxis and chemokine response). So Th2 responses predominate and they have high levels of IgE. They often have high eosinophil counts, candida infections, staph infections, and I'd assume a lacking response against TB if they were exposed.
 
Top