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Wolf, Y.* ; Shemer, A.* ; Polonsky, M.* ; Gross, M.* ; Mildner, A.* ; Yona, S.* ; David, E.* ; Kim, K.W.* ; Goldmann, T.* ; Amit, I.* ; Heikenwälder, M. ; Nedospasov, S.A.* ; Prinz, M.* ; Friedman, N.* ; Jung, S.*

Autonomous TNF is critical for in vivo monocyte survival in steady state and inflammation.

J. Exp. Med. 214, 905-917 (2017)
Verlagsversion DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Monocytes are circulating mononuclear phagocytes, poised to extravasate to sites of inflammation and differentiate into monocyte-derived macrophages and dendritic cells. Tumor necrosis factor (TNF) and its receptors are up-regulated during monopoiesis and expressed by circulating monocytes, as well as effector monocytes infiltrating certain sites of inflammation, such as the spinal cord, during experimental autoimmune encephalomyelitis (EAE). In this study, using competitive in vitro and in vivo assays, we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type counterpart. Moreover, monocyte-autonomous TNF is critical for the function of these cells, as TNF ablation in monocytes/macrophages, but not in microglia, delayed the onset of EAE in challenged animals and was associated with reduced acute spinal cord infiltration of Ly6Chi effector monocytes. Collectively, our data reveal a previously unappreciated critical cell-autonomous role of TNF on monocytes for their survival, maintenance, and function.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Quellenangaben Band: 214, Heft: 4, Seiten: 905-917 Artikelnummer: , Supplement: ,
Verlag Rockefeller University Press
Begutachtungsstatus Peer reviewed