Journal Article
Research Support, Non-U.S. Gov't
Add like
Add dislike
Add to saved papers

Differences in expression of cell surface co-stimulatory molecules, Toll-like receptor genes and secretion of IL-12 by bone marrow-derived dendritic cells from susceptible and resistant mouse strains in response to Coccidioides posadasii.

Cellular Immunology 2004 September
Coccidioides posadasii is a soil fungus that causes coccidioidomycosis or Valley Fever in the endemic regions of the southwestern US and Central America. Persons with decreased T cells reactivity and immune deficiency are at increased risk of developing severe disseminated infection. Among different mouse strains, DBA/2 mice are relatively resistant to C. posadasii whereas BALB/c mice are highly susceptible, and this discrepancy has been attributed to the difference in the development and expression of their Th1 cellular response. Dendritic cells (DC) are the most potent antigen-presenting cells that are activated after taking up pathogens or pathogens-derived antigens and regulate the immune response in the host, including Th1 cellular response. However, the DC responses against C. posadasii are not characterized. In the present study, we cultured bone-marrow derived DC (BMDC) from BALB/c and DBA/2 mice and infected with C. posadasii arthroconidia. The activation of BMDC was characterized by studying expression of cell surface co-stimulatory molecules (CD11c, MHC class II, CD40, CD80, and CD86), expression of genes encoding Toll-like receptors and release of IL-12. We found that the BMDC from DBA/2 mice showed significant upregulation of Toll-like receptor-2 and 4 genes expression, secretion of IL-12 (p<0.05) and modest increase in T cell co-stimulatory molecules as compared to BMDC from BALB/c mice. The data suggest that the differences in the activation status of DC in DBA/2 and BALB/c mice may be responsible for the discrepancy in their susceptibility to C. posadasii.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app