National Institutes of Health (NIH) scientists have identified a protein that plays matchmaker between two key types of white blood cells, T and B cells, enabling them to interact in a way that is crucial to establishing long-lasting immunity after an infection. Their finding may also explain why some individuals who have a genetic defect that prevents them from making this proteincalled SAPsuffer from lethal infections with a common virus that otherwise is rarely fatal (Epstein-Barr virus), while others with this genetic defect have problems with B-cell lymphomas.
The new study was a collaboration between the laboratories of NIH scientists Ronald Germain, M.D., Ph.D., at the National Institute of Allergy and Infectious Diseases (NIAID), and Pamela Schwartzberg, M.D., Ph.D., at the National Human Genome Research Institute (NHGRI). Their findings appear in the Oct. 9 issue of Nature.
When a B cell encounters a virus or other foreign agent, the B cell engulfs the virus and parts of it, called antigens, become displayed on the surface of the B cell. These antigens signal to T cells, which have specialized receptors that can bind to antigens on the B cells. Thus coupled, the T cells deliver signals that help B cells multiply and produce antibodies that will eventually destroy the offending virus. A critical tissue structure that facilitates these events is the germinal center, which normally forms after an infection within the lymph nodes, organs in which immune cells gather to carry out their functions.
"Understanding how B and T cells interact in the lymph nodes is crucial, because the germinal centers are the sites where long-lasting immunity begins," says NIAID Director Anthony S. Fauci, M.D. "If we can unravel how the body naturally builds defenses against repeat infections, it will aid us in developing more effective vaccines."
In some individuals, B cells do not make antibodies in response to infections and immu
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NIH/National Institute of Allergy and Infectious Diseases