• Georg F Weber, Benjamin G Chousterman, Ingo Hilgendorf, Clinton S Robbins, Igor Theurl, Louisa M S Gerhardt, Yoshiko Iwamoto, Tam D Quach, Muhammad Ali, John W Chen, Thomas L Rothstein, Matthias Nahrendorf, Ralph Weissleder, and Filip K Swirski.
• Center for Systems Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114 Department of Visceral, Thoracic and Vascular Surgery, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, 01307 Dresden, Germany fswirski@mgh.harvard.edu georg.weber@uniklinikum-dresden.de.
• J. Exp. Med. 2014 Jun 2;211(6):1243-56.

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.© 2014 Weber et al.

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