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Eskan, M.A.* ; Jotwani, R.* ; Abe, T.* ; Chmelar, J.* ; Lim, J.H.* ; Liang, S.* ; Ciero, P.A.* ; Krauss, J.L.* ; Li, F.* ; Rauner, M.* ; Hofbauer, L.C.* ; Choi, E.Y.* ; Chung, K.-J.* ; Hashim, A.* ; Curtis, M.A.* ; Chavakis, T.* ; Hajishengallis, G.*

The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss.

Nat. Immunol. 13, 465-473 (2012)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Aging is linked to greater susceptibility to chronic inflammatory diseases, several of which, including periodontitis, involve neutrophil-mediated tissue injury. Here we found that aging-associated periodontitis was accompanied by lower expression of Del-1, an endogenous inhibitor of neutrophil adhesion dependent on the integrin LFA-1, and by reciprocal higher expression of interleukin 17 (IL-17). Consistent with that, IL-17 inhibited gingival endothelial cell expression of Del-1, thereby promoting LFA-1-dependent recruitment of neutrophils. Young Del-1-deficient mice developed spontaneous periodontitis that featured excessive neutrophil infiltration and IL-17 expression; disease was prevented in mice doubly deficient in Del-1 and LFA-1 or in Del-1 and the IL-17 receptor. Locally administered Del-1 inhibited IL-17 production, neutrophil accumulation and bone loss. Therefore, Del-1 suppressed LFA-1-dependent recruitment of neutrophils and IL-17-triggered inflammatory pathology and may thus be a promising therapeutic agent for inflammatory diseases.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 1529-2908
e-ISSN 1529-2916
Zeitschrift Nature Immunology
Quellenangaben Band: 13, Heft: 5, Seiten: 465-473 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)