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- W2028138829 abstract "CD4 is a coreceptor on T helper (Th) cells that interacts with MHC class II molecules (MHCII). The mechanisms mediating the effects of CD4 on responses by T helper cells to stimulation of the antigen-specific T cell receptor (TCR) are still poorly understood. Here, we demonstrate T cell costimulation via CD4 signalling independent of T cell receptor-mediated signals. Incubation of T helper cells with peptide mimetics of the CD4-binding region on the MHC class II beta2 domain caused intracellular calcium mobilization in the absence of antigen or other T cell receptor stimuli. Engagement of CD4 by peptide mimetics or wild-type MHC class II, but not by mutant MHC class II molecules incapable of engaging CD4, inhibited the T cell receptor-mediated increase in cyclic AMP (cAMP) concentrations in T helper cells. CD4-mediated signals activated cyclic AMP phosphodiesterases (PDEs) and inhibited adenylyl cyclase. Full activation and clonal expansion of antigen-stimulated T helper cells required the CD4-mediated regulation of cyclic AMP. Our results suggest a costimulatory mechanism of CD4 function that acts on the second messengers, calcium and cyclic AMP." @default.
- W2028138829 created "2016-06-24" @default.
- W2028138829 creator A5025847228 @default.
- W2028138829 creator A5031605608 @default.
- W2028138829 date "2003-08-01" @default.
- W2028138829 modified "2023-09-23" @default.
- W2028138829 title "T cell receptor-independent CD4 signalling: CD4–MHC class II interactions regulate intracellular calcium and cyclic AMP" @default.
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- W2028138829 doi "https://doi.org/10.1016/s0898-6568(03)00037-8" @default.
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