The method that Staphylococcus aureus (staph) infection uses to inactivate the bodys immune response and cause previously healthy B cells to commit suicide, is described for the first time by researchers at the University of California, San Diego (UCSD) School of Medicine in the May 5, 2003 issue of the Journal of Experimental Medicine. The paper was selected for early online publication on April 28.
Normally, B cells mount an early defense against invading bacteria. From this immunologic experience, memory B cells are developed with the ability to quickly recognize these antigens and destroy the bacteria if they return in the future. When staph infections occur, however, this important process for immune defense can be corrupted.
In studies with mice, the researchers found that a staph protein, called SpA, acts like a B cell toxin because it mounts a pre-emptive attack to target a specific region on the antigen receptors of B cells, which ultimately causes their death. Although the B cells begin to respond, they are quickly shut down, as the SpA de-activates these B cell antigen receptors, and there is also loss of other surface molecules such as CD19 and CD21, which are important for amplifying immune responses. Then, within a few hours, the SpA toxin induces B cells to turn on themselves in a programmed suicide process called apoptosis. As a direct consequence, the B cells never get a chance to develop the memory cells necessary to recognize and fight future staph infections.
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