Kremer Kimberly N, Humphreys Troy D, Kumar Ashok, Qian Nan-Xin, Hedin Karen E
Department of Surgery, Mayo Graduate and Medical Schools, Mayo Clinic, Rochester, MN 55905, USA.
J Immunol. 2003 Jul 1;171(1):360-7. doi: 10.4049/jimmunol.171.1.360.
Stimulation of T lymphocytes with the ligand for the CXCR4 chemokine receptor stromal cell-derived factor-1alpha (SDF-1alpha/CXCL12), results in prolonged activation of the extracellular signal-regulated kinases (ERK) ERK1 and ERK2. Because SDF-1alpha is unique among several chemokines in its ability to stimulate prolonged ERK activation, this pathway is thought to mediate special functions of SDF-1alpha that are not shared with other chemokines. However, the molecular mechanisms of this response are poorly understood. In this study we show that SDF-1alpha stimulation of prolonged ERK activation in Jurkat T cells requires both the ZAP-70 tyrosine kinase and the Src homology 2 domain-containing leukocyte protein of 76 kDa (SLP-76) scaffold protein. This pathway involves ZAP-70-dependent tyrosine phosphorylation of SLP-76 at one or more of its tyrosines, 113, 128, and 145. Because TCR activates ERK via SLP-76-mediated activation of the linker of activated T cells (LAT) scaffold protein, we examined the role of LAT in SDF-1alpha-mediated ERK activation. However, neither the SLP-76 proline-rich domain that links to GADS and LAT, nor LAT, itself are required for SDF-1alpha to stimulate SLP-76 tyrosine phosphorylation or to activate ERK. Together, our results describe the distinct mechanism by which SDF-1alpha stimulates prolonged ERK activation in T cells and indicate that this pathway is specific for cells expressing both ZAP-70 and SLP-76.
用CXCR4趋化因子受体基质细胞衍生因子-1α(SDF-1α/CXCL12)的配体刺激T淋巴细胞,会导致细胞外信号调节激酶(ERK)ERK1和ERK2的长期激活。由于SDF-1α在几种趋化因子中,具有刺激ERK长期激活的独特能力,因此该信号通路被认为介导了SDF-1α的特殊功能,而这些功能是其他趋化因子所不具备的。然而,这种反应的分子机制尚不清楚。在本研究中,我们发现SDF-1α刺激Jurkat T细胞中ERK的长期激活,既需要ZAP-70酪氨酸激酶,也需要含Src同源2结构域的76 kDa白细胞蛋白(SLP-76)支架蛋白。该信号通路涉及ZAP-70依赖的SLP-76在其一个或多个酪氨酸位点(113、128和145)的酪氨酸磷酸化。由于T细胞受体通过SLP-76介导的活化T细胞连接蛋白(LAT)支架蛋白的激活来激活ERK,我们研究了LAT在SDF-1α介导的ERK激活中的作用。然而,无论是与GADS和LAT相连的SLP-76富含脯氨酸的结构域,还是LAT本身,都不是SDF-1α刺激SLP-76酪氨酸磷酸化或激活ERK所必需的。总之,我们的结果描述了SDF-1α刺激T细胞中ERK长期激活的独特机制,并表明该信号通路对同时表达ZAP-70和SLP-76的细胞具有特异性。