T Helper Cells Both Stimulate and Inhibit Germinal Centers of B-Cell Production; Better Understanding May Allow Amplification of Key Immune Responses and Diminishment of Autoimmune Reponses, Rockefeller Study Suggests

When we are exposed to a pathogen, the immune system’s B cells swarm to our lymph nodes, spleens, and tonsils. There, those cells mutate in germinal centers—microscopic boot camps that rush the B cells through volleys of mutations to produce the most potent antibodies for neutralizing the infectious agent. As long as a germinal center is up and running, B cells are free to mature and perfect their approach to fighting disease. But when a germinal center shuts down, usually after a few weeks, the training process grinds to a halt. Whatever antibodies happen to have formed by then are, for better or worse, the immune system’s final product.  Now,  a new study published in the July 16, 2021 issue of  Science describes one of the key elements involved in shutting down germinal centers. The findings may ultimately help scientists extend or cut short the length of time that germinal centers are active, with potential clinical implications. The article is titled” Expression of Foxp3 by T Follicular Helper Cells in End-Stage Germinal Centers.” “If we can make germinal centers last longer, maybe we can help the body form stronger antibodies in response to vaccines,” says Gabriel D. Victora (photo), PhD, Head of the Laboratory of Lymphocyte Dynamics at The Rockefeller University. “On the flipside, if we know how to shut down a germinal center, that may help treat autoimmune diseases which are caused by excessive immune responses.” 

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