| First Author | Tusche MW | Year | 2009 |
| Journal | J Exp Med | Volume | 206 |
| Issue | 12 | Pages | 2671-83 |
| PubMed ID | 19917778 | Mgi Jnum | J:155688 |
| Mgi Id | MGI:4415098 | Doi | 10.1084/jem.20091802 |
| Citation | Tusche MW, et al. (2009) Differential requirement of MALT1 for BAFF-induced outcomes in B cell subsets. J Exp Med 206(12):2671-83 |
| abstractText | B cell activation factor of the TNF family (BAFF) activates noncanonical nuclear factor kappaB (NF-kappaB) heterodimers that promote B cell survival. We show that although MALT1 is largely dispensable for canonical NF-kappaB signaling downstream of the B cell receptor, the absence of MALT1 results in impaired BAFF-induced phosphorylation of NF-kappaB2 (p100), p100 degradation, and RelB nuclear translocation in B220(+) B cells. This corresponds with impaired survival of MALT1(-/-) marginal zone (MZ) but not follicular B cells in response to BAFF stimulation in vitro. MALT1(-/-) MZ B cells also express higher amounts of TRAF3, a known negative regulator of BAFF receptor-mediated signaling, and TRAF3 was found to interact with MALT1. Furthermore, phenotypes associated with overexpression of BAFF, including increased MZ B cell numbers, elevated serum immunoglobulin titers, and spontaneous germinal center formation, were found to be dependent on B cell-intrinsic MALT1 expression. Our results demonstrate a novel role for MALT1 in biological outcomes induced by BAFF-mediated signal transduction. |
