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Interfering with Calcium Signaling to Inhibit Immune Responses
T cells of the immune system need increased intracellular calcium to become activated. The endoplasmic reticulum releases calcium in response to T cell receptor–mediated production of the second messenger IP3, which activates its receptor, the calcium channel IP3R. T cells lacking the guanine nucleotide exchange factor SLAT have defective calcium signaling. Fos et al. found that SLAT interacted with IP3R1 when T cells were stimulated, and the authors identified the regions in both proteins responsible for this interaction. Blocking this interaction with a cell-permeable fusion peptide corresponding to the interacting region of IP3R1 inhibited T cell function, which suggests that disrupting the SLAT-IP3R1 interaction may be a useful strategy for limiting excessive T cell activity in autoimmune or inflammatory diseases.
