| First Author | Blonska M | Year | 2013 |
| Journal | Sci Signal | Volume | 6 |
| Issue | 306 | Pages | ra110 |
| PubMed ID | 24345681 | Mgi Jnum | J:259782 |
| Mgi Id | MGI:6142772 | Doi | 10.1126/scisignal.2004273 |
| Citation | Blonska M, et al. (2013) Activation of the transcription factor c-Maf in T cells is dependent on the CARMA1-IKKbeta signaling cascade. Sci Signal 6(306):ra110 |
| abstractText | The proto-oncogene c-Maf is a transcription factor that plays a critical role in the differentiation of various T helper (T(H)) cell subsets. The amount of c-Maf increases after stimulation of the T cell receptor (TCR), which results in the production of multiple cytokines. We showed that two essential regulators of the transcription factor nuclear factor kappaB (NF-kappaB), the scaffold protein CARMA1 and the kinase IKKbeta [inhibitor of NF-kappaB (IkappaB) kinase beta], are also critical for the activation of c-Maf. Although CARMA1 deficiency did not affect the TCR-dependent increase in c-Maf abundance in T cells, CARMA1-dependent activation of the IKK complex was required for the nuclear translocation of c-Maf and its binding to the promoters of its target genes. Consistent with a role for c-Maf in the development of T follicular helper (T(FH)) cells, which provide help to B cells in the germinal centers of the spleen, CARMA1- or IKKbeta-deficient mice immunized with peptide antigen had defects in the generation of T(FH) cells, formation of germinal centers, and production of antigen-specific antibodies. Together, these data suggest a mechanism by which c-Maf is regulated during T cell activation and differentiation. |
