Pleural innate response activator B cells protect against pneumonia via a GM-CSF-IgM axis
Weber, Georg F.
Robbins, Clinton S.
Gerhardt, Louisa M.S.
Quach, Tam D.
Rothstein, Thomas L.
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CitationWeber, G. F., B. G. Chousterman, I. Hilgendorf, C. S. Robbins, I. Theurl, L. M. Gerhardt, Y. Iwamoto, et al. 2014. “Pleural innate response activator B cells protect against pneumonia via a GM-CSF-IgM axis.” The Journal of Experimental Medicine 211 (6): 1243-1256. doi:10.1084/jem.20131471. http://dx.doi.org/10.1084/jem.20131471.
AbstractPneumonia 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.
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