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Maintenance of a memory cell population is thought to be independent of antigen. However, it has now been shown that unless memory cells get some signals via MHC, they become functionally defective.
CD8+ TS cells induce antigen-specific tolerance. The TS cells may do this by increasing the expression of inhibitory receptor ILT3 and ILT4 on DCs, rendering these cells toleregenic to CD4 cells.
Gonococci that bind the coinhibitory receptor CEACAM1 appear to down-regulate the activation and proliferation of CD4+ T cells. Such infection-induced immunosuppression helps explain why there is little specific immune response associated with gonococcal disease.
The biochemical events that mediate inside-out signaling to β1 and β2 integrin receptors after TCR ligation are poorly understood. Using a transgenic mouse model, investigators have implicated an unexpected candidate, Rap1, as a key mediator of inside-out signaling in activated T cells.
The development of new experimental tools is helping to unravel the molecular secrets of cell differentiation. The identification, by gene chip technology, of a HMG box protein called TOX has yielded valuable information about thymocyte differentiation.
One of the major goals of the WHO is elimination of polio, but the nature of rapidly evolving enteroviruses makes this task more complex than it initially appears.