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Dynamics of MHC Class II-Activating Signals in Murine Resting B Cells¹

Albany Medical College, Center for Immunology and Microbial Disease, Albany, NY 12208

MHC class II (MHC II) proteins are competent signaling molecules on APC. However, little is known about the mechanisms that control generation of their activating signals. Previous reports highlighted a number of factors that could affect the nature and outcome of MHC II signals, including the inability of MHC II ligation on resting vs activated murine B cells to induce mobilization of Ca²⁺. In the present study, we report that ligation of MHC II on resting murine B cells reproducibly induces mobilization of intracellular Ca²⁺ using both mAbs and cognate T cells as ligands. Mobilization of Ca²⁺ was independent of MHC II haplotype, isotype, or mouse genetic background. MHC II-mediated mobilization of Ca²⁺ is completely inhibited by inhibitors of src-like kinases and syk, and MHC II ligation increases overall tyrosine phosphorylation level. Moreover, MHC II ligation results in specific up-regulation of CD86. However, induction of these responses is dependent on the type of anti-MHC II Ab used, suggesting that epitope specificity and/or the nature of ligation is important. Moreover, we demonstrate that MHC II-derived signals are strictly regulated by the order and timing of BCR and CD40 signals, suggesting coordination of these signals preserves the integrity of early B cell priming events. Thus, the mode and the context of MHC II ligation influence generation of MHC II-derived activating signals in resting B cells. Based on these results, a new model that highlights the role of MHC II-activating signals in regulation of Ag presentation by B cells is proposed.

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