The protein known as SLAT (SWAP-70?like adaptor of T cells) was recently identified, however it?s physiological function remained unclear.
In a study appearing online on July 26 in advance of publication in the August print issue of the Journal of Clinical Investigation, Amnon Altman and colleagues from the La Jolla Institute for Allergy and Immunology studied SLAT-/- mice and found that these animals displayed defects in the early stages of thymocyte development.
Thymocytes are precursors of immune cells known as T cells, which respond to foreign pathogens and are tolerant of self-antigens. The observed defect in thymocyte development resulted in reduced numbers of peripheral T cells. In addition, the thymocytes in these animals were impaired in their ability to differentiate into Th1- or Th2-type cells, and as such Th1- and Th2-type inflammatory immune responses in the lung were also impaired. The authors went on to show that the basis for this defect is that SLAT-deficient T cells are incapable of releasing calcium in response to stimulation, which limits their ability to further differentiate. These data suggest that SLAT plays an important role in fundamental aspects of T cell development and physiology.
TITLE: SLAT regulates Th1 and Th2 inflammatory responses by controlling Ca2+/NFAT signaling