| First Author | Sriskantharajah S | Year | 2009 |
| Journal | Nat Immunol | Volume | 10 |
| Issue | 1 | Pages | 38-47 |
| PubMed ID | 19060899 | Mgi Jnum | J:142340 |
| Mgi Id | MGI:3821396 | Doi | 10.1038/ni.1685 |
| Citation | Sriskantharajah S, et al. (2009) Proteolysis of NF-kappaB1 p105 is essential for T cell antigen receptor-induced proliferation. Nat Immunol 10(1):38-47 |
| abstractText | To investigate the importance of proteolysis of NF-kappaB1 p105 induced by the kinase IKK in activation of the transcription factor NF-kappaB, we generated 'Nfkb1(SSAA/SSAA)' mice, in which the IKK-target serine residues of p105 were substituted with alanine. Nfkb1(SSAA/SSAA) mice had far fewer CD4+ regulatory and memory T cells because of cell-autonomous defects. These T cell subtypes require activation of NF-kappaB by the T cell antigen receptor for their generation, and the Nfkb1(SSAA) mutation resulted in less activation of NF-kappaB in CD4+ T cells and proliferation of CD4+ T cells after stimulation of the T cell antigen receptor. The Nfkb1(SSAA) mutation also blocked the ability of CD4+ T cells to provide help to wild-type B cells during a primary antibody response. IKK-induced p105 proteolysis is therefore essential for optimal T cell antigen receptor-induced activation of NF-kappaB and mature CD4+ T cell function. |
