Essential role for IKKγ/NEMO in TCR‐induced IL‐2 expression in Jurkat T cells

• Published in: European journal of immunology Vol. 33; no. 7; pp. 1917 - 1924
• Main Authors: He, Kai‐Li, Ting, Adrian T.
• Format: Journal Article
• Language: English
• Published: Weinheim WILEY‐VCH Verlag 01.07.2003
• Subjects: IKKγ/NEMO; IL‐2; NF‐κB; Signaling; TCR
• ISSN: 0014-2980; 1521-4141
• DOI: 10.1002/eji.200323650

The control of IL‐2 gene expression in T cells by multiple transcriptional factors has been extensively explored, however, the role of the NF‐κB signaling pathway in TCR‐dependent IL‐2 production still remains unclear. In this study, we used a somatic cell genetics approach to address this question. Triggering TCR in mutant Jurkat T cells lacking IKKγ/NEMO failed to induce IL‐2due to a selective loss in I‐κB kinase activity, I‐κBα degradation and NF‐κB DNA‐binding activity. The AP‐1 and NF‐AT binding activities in the IL‐2 promoter were comparable between wild‐type and mutant T cells. These defects in the mutant cell line were rescued by the reintroduction of exogenous IKKγ. Taken together, our data demonstrate that IKKγ plays an essential role in TCR‐induced signaling pathways leading to IL‐2 expression.