Scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, have demonstrated why certain immune cells chronically exposed to HIV shut down, and how they can be reactivated.
Healthy B cells have a balanced mix of surface proteins that the immune system can use, like the gas pedal and brake of a car, either to activate the cell or to damp down its activity. However, in people with long-term HIV infection who have not begun antiretroviral therapy, their B cells—responsible for producing anti-HIV antibodies—display a surplus of inhibitory receptors, the surface proteins used to apply the brakes on a B cell. Scientists from the NIAID Laboratory of Immunoregulation led by Lela Kardava, Ph.D., Susan Moir, Ph.D., and Anthony S. Fauci, M.D., NIAID Director and Chief of the laboratory, wanted to know if this phenomenon can help explain why B cells become "exhausted" and essentially shut down in people who are HIV-infected but treatment-naive.
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