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Dectin-3 Deficiency Promotes Colitis Development due to Impaired Antifungal Innate Immune Responses in the Gut
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نویسنده
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wang t. ,pan d. ,zhou z. ,you y. ,jiang c. ,zhao x. ,lin x.
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منبع
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plos pathogens - 2016 - دوره : 12 - شماره : 6
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چکیده
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Interactions between commensal fungi and gut immune system are critical for establishing colonic homeostasis. here we found that mice deficient in dectin-3 (clec4d-/-),a c-type lectin receptor that senses fungal infection,were more susceptible to dextran sodium sulfate (dss)-induced colitis compared with wild-type mice. the specific fungal burden of candida (c.) tropicalis was markedly increased in the gut after dss treatment in clec4d-/- mice,and supplementation with c. tropicalis aggravated colitis only in clec4d-/- mice,but not in wild-type controls. mechanistically,dectin-3 deficiency impairs phagocytic and fungicidal abilities of macrophages,and c. tropicalis-induced nf-κb activation and cytokine production. the conditioned media derived from dectin-3-deficient macrophages were defective in promoting tissue repairing in colonic epithelial cells. finally,anti-fungal therapy was effective in treating colitis in clec4d-/- mice. these studies identified the role of dectin-3 and its functional interaction with commensal fungi in intestinal immune system and regulation of colonic homeostasis. © 2016 wang et al.
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آدرس
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department of molecular and cellular oncology,the university of texas,md anderson cancer center,houston,tx,united states,the state key laboratory of pharmaceutical biotechnology,division of immunology,medical school,nanjing university,nanjing, China, department of molecular and cellular oncology,the university of texas,md anderson cancer center,houston,tx,united states,cancer biology program,the university of texas,graduate school of biomedical sciences,houston,tx, United States, department of molecular and cellular oncology,the university of texas,md anderson cancer center,houston,tx,united states,cancer biology program,the university of texas,graduate school of biomedical sciences,houston,tx, United States, department of molecular and cellular oncology,the university of texas,md anderson cancer center,houston,tx, United States, department of molecular and cellular oncology,the university of texas,md anderson cancer center,houston,tx, United States, institute for immunology,tsinghua university school of medicine,beijing, China, department of molecular and cellular oncology,the university of texas,md anderson cancer center,houston,tx,united states,cancer biology program,the university of texas,graduate school of biomedical sciences,houston,tx,united states,institute for immunology,tsinghua university school of medicine,beijing, China
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Authors
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