Differential roles for Wiskott-Aldrich syndrome protein in immune synapse formation and IL-2 production
Differential roles for Wiskott-Aldrich syndrome protein in immune synapse formation and IL-2 production
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DOI：
10.4049/jimmunol.173.3.1658
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发表时间：
2004-08-01
影响因子：
4.4
通讯作者：
Burkhardt, JK
中科院分区：
文献类型：
--
作者：
Cannon, JL;Burkhardt, JK
Wiskott-Aldrich综合征蛋白（WASP）缺陷的T细胞表现出IL-2产生缺陷，这被广泛认为是源于肌动蛋白重塑和免疫突触形成的原发性缺陷。然而，令人惊讶的是，我们发现wasp缺陷T细胞对ag特异性apc有反应，可正常聚合肌动蛋白并组织talin和PKCtheta，形成至少稳定3小时的免疫突触。在低剂量的肽下，wasp缺陷T细胞表现出较低的talin和PKCtheta极化效率。因此，尽管WASP可能在低肽浓度下促进免疫突触的形成，但这一过程并不需要WASP。即使在免疫突触形成正常的情况下，也可以观察到IL-2产生的缺陷，这表明WASP在调节IL-2产生中的作用独立于其在免疫突触形成中的作用。
Wiskott-Aldrich syndrome protein (WASP)-deficient T cells exhibit defects in IL-2 production that are widely believed to stem from primary defects in actin remodeling and immune synapse formation. Surprisingly, however, we find that WASP-deficient T cells responding to Ag-specific APCs polymerize actin and organize talin and PKCtheta normally, forming an immune synapse that is stable for at least 3 h. At low doses of peptide, WASP-deficient T cells show less efficient talin and PKCtheta polarization. Thus, although WASP may facilitate immune synapse formation at low peptide concentrations, WASP is not required for this process. Defects in IL-2 production are observed even under conditions in which immune synapse formation proceeds normally, suggesting that the role of WASP in regulating IL-2 production is independent of its role in immune synapse formation.