| First Author | Wang H | Year | 2023 |
| Journal | Immunohorizons | Volume | 7 |
| Issue | 8 | Pages | 587-599 |
| PubMed ID | 37610299 | Mgi Jnum | J:358471 |
| Mgi Id | MGI:7780300 | Doi | 10.4049/immunohorizons.2300038 |
| Citation | Wang H, et al. (2023) MAVS Positively Regulates Mitochondrial Integrity and Metabolic Fitness in B Cells. Immunohorizons 7(8):587-599 |
| abstractText | Activated B cells experience metabolic changes that require mitochondrial remodeling, in a process incompletely defined. In this study, we report that mitochondrial antiviral signaling protein (MAVS) is involved in BCR-initiated cellular proliferation and prolonged survival. MAVS is well known as a mitochondrial-tethered signaling adaptor with a central role in viral RNA-sensing pathways that induce type I IFN. The role of MAVS downstream of BCR stimulation was recognized in absence of IFN, indicative of a path for MAVS activation that is independent of viral infection. Mitochondria of BCR-activated MAVS-deficient mouse B cells exhibited a damaged phenotype including disrupted mitochondrial morphology, excess mitophagy, and the temporal progressive blunting of mitochondrial oxidative capacity with mitochondrial hyperpolarization and cell death. Costimulation of MAVS-deficient B cells with anti-CD40, in addition to BCR stimulation, partially corrected the mitochondrial structural defects and functionality. Our data reveal a (to our knowledge) previously unrecognized role of MAVS in controlling the metabolic fitness of B cells, most noticeable in the absence of costimulatory help. |
