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by Leigh MacMillan | Posted on Wednesday, Jan. 15, 2014 — 8:00 AM
Infection with HIV-1 (human immunodeficiency virus type 1) induces defects in both cellular and humoral (antibody) immune responses. To understand the extent of antibody-producing B cell dysfunction during HIV-1 infection, Spyros Kalams, M.D., associate professor of Medicine, and colleagues studied B cells from HIV-infected and HIV-negative individuals.
They found that B cells from HIV-infected individuals with higher viral loads had higher baseline expression of the activation marker CD86 and decreased ability to respond to HIV-1 in vitro. They also showed that B cells from HIV-infected individuals had higher expression of the inhibitory molecule PD-1 and that PD-1 blockade improved B cell responsiveness to HIV-1.
The findings, reported Dec. 16 in PLOS ONE, demonstrate that during chronic HIV-1 infection, B cells are activated but lose their full capacity to respond to antigen. The results also show that suppression of inhibitory molecules (along with a robust helper T cell response) may help preserve B cell function, which could have implications for HIV vaccine development.
This research was supported by grants from the National Institutes of Health (AI078064, AI089554).
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Health and Medicine, Reporter, Research Aliquots, Department of Medicine, HIV, immune response, NIAID, NIH, pathology microbiology and immunology, Plos ONE, Reporter Jan 10 2014, Spyros Kalams, vaccine
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