The complement system in the airway epithelium: An overlooked host defense mechanism and therapeutic target? - 04/05/18
Key words : Complement, allergic rhinitis, properdin, epithelial cells, asthma, ovalbumin, cystic fibrosis, bronchiolitis, pulmonary fibrosis, anaphylatoxins
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Supported by the National Institutes of Health (NIH; R01 GM0099111 to J.P.A. and R01HL122585 to S.L.B.) and NIH training grants in the Principles of Pulmonary Research (5T32 HL007317 to H.S.K., and the Immunobiology of Rheumatic Diseases (5T32-AR007279 to H.S.K.). Research reported in this publication is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, part of the NIH (P30AR048335); an NIH grant for the Washington University Institute of Clinical and Translational Sciences (3UL1 TR000448); and the Hubert C. and Dorothy R. Moog Professorship (to S.L.B.) supported by the Barnes-Jewish Hospital Foundation. |
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Disclosure of potential conflict of interest: J. P. Atkinson has received grants from the National Institutes of Health (2 R01 GM099111 and R21 AR069833) and the Rheumatology Research Foundation; has board memberships with Compliment Corporation, Kypha Inc, and Gemini Therapeutics; has consultant arrangements with Achillion Pharmaceuticals, BioMarin Pharmaceuticals, Annexon Biosciences, Celldex Therapeutics, Clinical Pharmacy Services CDMI, Kypha Inc, Omeros Corporation, and True North Therapeutics; and receives stock/stock options from Compliment Corporation, Kypha Inc, and Gemini Therapeutics. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 141 - N° 5
P. 1582 - mai 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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