| First Author | Schmidt-Supprian M | Year | 2004 |
| Journal | J Immunol | Volume | 173 |
| Issue | 3 | Pages | 1612-9 |
| PubMed ID | 15265889 | Mgi Jnum | J:92037 |
| Mgi Id | MGI:3051486 | Doi | 10.4049/jimmunol.173.3.1612 |
| Citation | Schmidt-Supprian M, et al. (2004) I kappa B kinase 2 deficiency in T cells leads to defects in priming, B cell help, germinal center reactions, and homeostatic expansion. J Immunol 173(3):1612-9 |
| abstractText | Signal transduction from proinflammatory stimuli leading to NF-kappa B-dependent gene expression is mediated by the I kappa B kinase 2 (IKK2/IKK beta). Therefore, IKK2 has become an important drug target for treatment of inflammatory conditions. T cells, whose activation depends to a large extent on the activity of NF-kappa B transcription factors, play important roles in inflammation and autoimmunity. Ablation of IKK2 specifically in T cells in CD4cre/Ikk2(FL) mice allows their survival and activation by polyclonal stimuli in vitro, suggesting that IKK2 is dispensable for T cell activation. We report in this study that IKK2-deficient T cells expand efficiently in response to superantigen administration in vivo, but are completely deficient in recall responses, most likely due to inefficient priming. IKK2-deficient T cells provide suboptimal B cell help and fail to support germinal center reactions. Finally, IKK2 is essential for homeostatic expansion of naive T cells, reflected by the inability of IKK2-deficient T cells to induce colitis in lymphopenic hosts. |
