First Author | Peterson EJ | Year | 1999 |
Journal | Eur J Immunol | Volume | 29 |
Issue | 7 | Pages | 2223-32 |
PubMed ID | 10427985 | Mgi Jnum | J:56584 |
Mgi Id | MGI:1341951 | Doi | 10.1002/(SICI)1521-4141(199907)29:07<2223::AID-IMMU2223>3.0.CO;2-6 |
Citation | Peterson EJ, et al. (1999) NK cytokine secretion and cytotoxicity occur independently of the SLP-76 adaptor protein. Eur J Immunol 29(7):2223-32 |
abstractText | The adapter protein SLP-76 is required for T cell development and TCR signal transduction. SLP-76 is also expressed in NK cells, yet splenic populations of NK cells develop normally in SLP-76-deficient mice. We examined the effects of SLP-76 deficiency upon cellular activation through studies of NK function in SLP-76(-/-) mice. This study presents evidence that NK populations in both spleen and liver of SLP-76(-/-) mice remain intact. Natural cytotoxic responses of SLP-76(-/-) splenocytes proceed in a manner comparable to those of wild-type control splenocytes. Similar to controls, SLP-76(-/-) splenocytes exhibit enhanced survival and augmented cytotoxic capacity after in vitro culture with IL-2. IL-2-stimulated SLP-76(-/-) splenocytes also retain normal antibody-dependent cellular cytotoxicity and the ability to secrete IFN-gamma in response to IL-12 stimulation. These results indicate that, unlike events stimulated by TCR engagement, signaling cascades engaged by IL-2 and IL-12 receptors, by Fc gammaRIIIA (which mediates antibody-dependent cellular cytotoxicity), and by natural cytotoxicity-associated receptors on murine NK cells can occur independently of SLP-76. |