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T cells

New regulator of calcium signalling

Nature Reviews Immunology volume 7, page 663 (2007)Cite this article

SLAT (also known as IBP) is a guanine-nucleotide-exchange factor that is known to be activated following ligation of the T-cell receptor (TCR). To investigate the physiological role of SLAT in T cells, Bécart et al. studied T-cell development in SLAT-deficient mice. Their analysis revealed that there was a defect at an early stage of thymocyte development in Slat−/− mice, such that proliferation of thymocytes at the double negative 1 (DN1) stage was impaired. As a result, fewer CD4+ T cells and, to a lesser extent, CD8+ T cells were present in the periphery of Slat−/− mice compared with wild-type mice.

Moreover, those CD4+ T cells that did populate the periphery in Slat−/− mice showed markedly reduced proliferation and interleukin-2 production in response to TCR and CD28 ligation, although they proliferated normally in response to PMA (phorbol 12-myristate 13-acetate) plus ionomycin (stimuli known to bypass the TCR).

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References

ORIGINAL RESEARCH PAPER

  1. Bécart, S. et al. SLAT regulates Th1 and Th2 inflammatory responses by controlling Ca2+/NFAT signaling. J. Clin. Invest. 117, 2164–2175 (2007)

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FURTHER READING

  1. Feske, S. Calcium signalling in lymphocyte activation and disease. Nature Rev. Immunol. 7, 690–702 (2007)

    Article  CAS  Google Scholar 

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Authors
  1. Lucy Bird
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Bird, L. New regulator of calcium signalling. Nat Rev Immunol 7, 663 (2007). https://doi.org/10.1038/nri2169

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  • DOI: https://doi.org/10.1038/nri2169

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