| First Author | Chikuma S | Year | 2012 |
| Journal | Nat Immunol | Volume | 13 |
| Issue | 6 | Pages | 596-603 |
| PubMed ID | 22544392 | Mgi Jnum | J:186453 |
| Mgi Id | MGI:5432328 | Doi | 10.1038/ni.2293 |
| Citation | Chikuma S, et al. (2012) TRIM28 prevents autoinflammatory T cell development in vivo. Nat Immunol 13(6):596-603 |
| abstractText | TRIM28 is a component of heterochromatin complexes whose function in the immune system is unknown. By studying mice with conditional T cell-specific deletion of TRIM28 (CKO mice), we found that TRIM28 was phosphorylated after stimulation via the T cell antigen receptor (TCR) and was involved in the global regulation of CD4(+) T cells. The CKO mice had a spontaneous autoimmune phenotype that was due in part to early lymphopenia associated with a defect in the production of interleukin 2 (IL-2) as well as incomplete cell-cycle progression of their T cells. In addition, CKO T cells showed derepression of the cytokine TGF-beta3, which resulted in an altered cytokine balance; this caused the accumulation of autoreactive cells of the T(H)17 subset of helper T cells and of Foxp3(+) T cells. Notably, CKO Foxp3(+) T cells were unable to prevent the autoimmune phenotype in vivo. Our results show critical roles for TRIM28 in both T cell activation and T cell tolerance. |
