| First Author | Mufazalov IA | Year | 2017 |
| Journal | Eur J Immunol | Volume | 47 |
| Issue | 8 | Pages | 1335-1341 |
| PubMed ID | 28598502 | Mgi Jnum | J:245503 |
| Mgi Id | MGI:5916221 | Doi | 10.1002/eji.201746933 |
| Citation | Mufazalov IA, et al. (2017) Balanced Bcl-3 expression in murine CD4+ T cells is required for generation of encephalitogenic Th17 cells. Eur J Immunol 47(8):1335-1341 |
| abstractText | The function of NF-kappaB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl-3, an atypical member of the IkappaB family. By using a murine model of conditional Bcl-3 overexpression specifically in T cells, we observed impairment in the development of Th2, Th1, and Th17 cells. High expression of Bcl-3 promoted CD4+ T-cell survival, but at the same time suppressed proliferation in response to TCR stimulation, resulting in reduced CD4+ T-cell expansion. As a consequence, T-cell-specific overexpression of Bcl-3 led to reduced inflammation in the small intestine of mice applied with anti-CD3 in a model of gut inflammation. Moreover, impaired Th17-cell development resulted in the resistance of Bcl-3 overexpressing mice to EAE, a mouse model of multiple sclerosis. Thus, we concluded that fine-tuning expression of Bcl-3 is needed for proper CD4+ T-cell development and is required to sustain Th17-cell mediated pathology. |
