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Weber, G.F.* ; Chousterman, B.G.* ; He, S.* ; Fenn, A.M.* ; Nairz, M.* ; Anzai, A.* ; Brenner, T.* ; Uhle, F.* ; Iwamoto, Y.* ; Robbins, C.S.* ; Noiret, L.* ; Maier, S.L.* ; Zönnchen, T.* ; Rahbari, N.N.* ; Schölch, S.* ; Klotzsche-von Ameln, A.* ; Chavakis, T.* ; Weitz, J.* ; Hofer, S.* ; Weigand, M.A.* ; Nahrendorf, M.* ; Weissleder, R.* ; Swirski, F.K.*

Interleukin-3 amplifies acute inflammation and is a potential therapeutic target in sepsis.

Science 347, 1260-1265 (2015)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Sepsis is a frequently fatal condition characterized by an uncontrolled and harmful host reaction to microbial infection. Despite the prevalence and severity of sepsis, we lack a fundamental grasp of its pathophysiology. Here we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis. Using a mouse model of abdominal sepsis, we showed that innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6C(high) monocytes and neutrophils and fuels a cytokine storm. IL-3 deficiency protects mice against sepsis. In humans with sepsis, high plasma IL-3 levels are associated with high mortality even after adjusting for prognostic indicators. This study deepens our understanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and reveals a new therapeutic target for treating sepsis.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0036-8075
e-ISSN 1095-9203
Zeitschrift Science
Quellenangaben Band: 347, Heft: 6227, Seiten: 1260-1265 Artikelnummer: , Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)