T cell survival protein controls gene activity, offering clues to HIV persistence
A prominent protein on most human cells may be key to unlocking the code that makes humans susceptible to pathogenic bacteria and viruses, including human immunodeficiency virus (HIV), according to a new study published in Science Immunology led by researchers at Purdue University and the National Heart, Lung, and Blood Institute.
A recently discovered protein called CD46 plays a crucial role in controlling gene activity in human T cells, offering insights into why some people remain persistently infected with HIV despite antiretroviral therapy. This finding, published in Science Immunology, challenges the belief that CD46 primarily serves as an entry point for pathogens, revealing instead that it functions as a "safety switch" to prevent T cells from dying.
CD46 helps T cells obtain necessary nutrients to function and prevents naive T cells from self-destructing during normal programmed cell death. The study, co-led by Purdue University's Majid Kazemian and NHLBI's Claudia Kemper, demonstrates that CD46 controls T cell survival, response to infection, and regulation of viral gene activity.
Without CD46 signaling, naive T cells succumb to cell death, hindering their ability to mount an effective immune response. Understanding CD46's role could lead to new therapies for immune deficiencies, infectious diseases, and inflammatory disorders, including HIV. The research highlights the complement system's broader functions beyond pathogen elimination, acting as a communication system that informs immune cells about energy use, metabolism, and inflammation.
This discovery underscores the importance of comprehending the basic mechanisms that govern immune cell function for translational research in various medical fields.
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