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. 2005 Mar 15;174(6):3153-7.
doi: 10.4049/jimmunol.174.6.3153.

Signaling lymphocytic activation molecule-associated protein controls NKT cell functions (V体育安卓版)

Brian Chung  1 , Ala Aoukaty, Jan Dutz, Cox Terhorst, Rusung Tan
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Signaling lymphocytic activation molecule-associated protein controls NKT cell functions

Brian Chung et al. J Immunol. .

Abstract

X-linked lymphoproliferative disease (XLP) is a fatal immunological disorder that typically manifests following EBV infection. XLP patients exhibit a number of immune defects including abnormal T, B, and NK lymphocyte function. These defects have been attributed to mutations of Src homology 2 domain-containing gene 1A (SH2D1A), the gene encoding signaling lymphocytic activation molecule-associated protein (SAP), an intracellular adaptor molecule expressed in lymphocytes. We have observed that SAP knockout (SAPKO) mice and humans with XLP have a complete lack of CD1d-restricted NKT cells. As expected, SAPKO mice injected with the NKT cell agonist, alpha-galactosylceramide failed to generate NKT cell IFN-gamma or IL-4. Furthermore, in contrast to wild-type littermates, SAPKO mice coinjected with OVA and alpha-galactosylceramide failed to mount OVA-specific CTL responses VSports手机版. These data suggest that an absence of NKT cells may underlie part of the immune dysregulation seen in SAPKO mice and in XLP patients. .

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