| First Author | Akkaya M | Year | 2018 |
| Journal | Nat Immunol | Volume | 19 |
| Issue | 8 | Pages | 871-884 |
| PubMed ID | 29988090 | Mgi Jnum | J:282387 |
| Mgi Id | MGI:6380778 | Doi | 10.1038/s41590-018-0156-5 |
| Citation | Akkaya M, et al. (2018) Second signals rescue B cells from activation-induced mitochondrial dysfunction and death. Nat Immunol 19(8):871-884 |
| abstractText | B cells are activated by two temporally distinct signals, the first provided by the binding of antigen to the B cell antigen receptor (BCR), and the second provided by helper T cells. Here we found that B cells responded to antigen by rapidly increasing their metabolic activity, including both oxidative phosphorylation and glycolysis. In the absence of a second signal, B cells progressively lost mitochondrial function and glycolytic capacity, which led to apoptosis. Mitochondrial dysfunction was a result of the gradual accumulation of intracellular calcium through calcium response-activated calcium channels that, for approximately 9 h after the binding of B cell antigens, was preventable by either helper T cells or signaling via the receptor TLR9. Thus, BCR signaling seems to activate a metabolic program that imposes a limited time frame during which B cells either receive a second signal and survive or are eliminated. |
