| First Author | Weber GF | Year | 2014 |
| Journal | J Exp Med | Volume | 211 |
| Issue | 6 | Pages | 1243-56 |
| PubMed ID | 24821911 | Mgi Jnum | J:213739 |
| Mgi Id | MGI:5585690 | Doi | 10.1084/jem.20131471 |
| Citation | Weber GF, et al. (2014) Pleural innate response activator B cells protect against pneumonia via a GM-CSF-IgM axis. J Exp Med 211(6):1243-56 |
| abstractText | Pneumonia is a major cause of mortality worldwide and a serious problem in critical care medicine, but the immunophysiological processes that confer either protection or morbidity are not completely understood. We show that in response to lung infection, B1a B cells migrate from the pleural space to the lung parenchyma to secrete polyreactive emergency immunoglobulin M (IgM). The process requires innate response activator (IRA) B cells, a transitional B1a-derived inflammatory subset which controls IgM production via autocrine granulocyte/macrophage colony-stimulating factor (GM-CSF) signaling. The strategic location of these cells, coupled with the capacity to produce GM-CSF-dependent IgM, ensures effective early frontline defense against bacteria invading the lungs. The study describes a previously unrecognized GM-CSF-IgM axis and positions IRA B cells as orchestrators of protective IgM immunity. |
