In Leishmania major infection, the Th1 and Th2 response is associated with healing and non-healing in experimental models respectively. Increases in CD86 expression on monocytes/macrophages has been associated with the establishment of the disease, and treatment of mice with anti-CD86 blocking antibody leads to decreased parasite burdens accompanied by a decrease in Th2 cytokines. Are there any reports to show that CD86 (B7.2) plays a direct role in Th2 polarisation? And has there been any link between CD80 (B7.1) expression and a Th1 profile, particularly during Leishmania infection?
Hi Amy, I was once interested in this topic while studying the immune changes after stroke in humans, but apparently there are diverse results depending on whether you do in vitro or in vivo studies. I'm sure there is more literature on this but you can check the results and the discussion of this study in rats.
http://www.ncbi.nlm.nih.gov/pubmed/11696200
Thank you, I was reading a lot of conflicting reports depending on the disease studied.
Dear Amy there is a big difference in signal transduction generated with CD3 CD28 activation as compare to CD3 only. Usually CD3 activation induces around half of the signal transduction metabolites required for a complete activation. However, in naive T cells, essentially CD3/CD28 activation would render Th0 cells, in the begining, then dependenin on the cytokine milleau you can induce preferentially GATA3 or t.Bet so the question would rather be are you refering to skin infection by Leishmania? If so then the response would be dependent upon Langerhan cell activation. I would recommend that you read papers by Felix Tapia and Martin Olivier which have conducted such studies in different models, thay are both members of Research Gate. Regards
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