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IMSUT & RCASTGCOE Program Seminar

Date and Time: January 27th &s_comma; 2011 16 :00 17:00 pm

Venue : General Research Building&s_comma; 4F conference room&s_comma; Institute of Medical Science&s_comma; University of Tokyo

Speaker:Dr. Mi-Na Kweon&s_comma; Ph.D.&s_comma; Chief Scientist

Mucosal Immunology Section&s_comma; International Vaccine Institute (Country) Korea

Seminar Title:Type I Interferon Signaling Regulates Ly6Chi Monocytes and Neutrophils during Acute Viral Pneumonia in Mice 

(Language) English

Summary:Type I interferon (IFN-I) plays a critical role in the homeostasis of hematopoietic stem cells and influences neutrophil influx to the site of inflammation. IFN-I receptor knockout (Ifnar1-/-) mice develop significant defects in the infiltration of Ly6Chi monocytes in the lung after influenza infection (A/PR/8/34&s_comma; H1N1). Ly6Chi monocytes of wild-type (WT) mice are the main producers of MCP-1 while the alternatively generated Ly6Cint monocytes of Ifnar1-/- mice mainly produce KC for neutrophil influx. As a consequence&s_comma; Ifnar1-/- mice recruit more neutrophils after influenza infection than do WT mice. Treatment of IFNAR1 blocking antibody on the WT bone marrow (BM) cells in vitro failed to differentiate into Ly6Chi monocytes. By using BM chimeric mice (WT BM into Ifnar1-/- and vice versa)&s_comma; we confirmed that IFN-I signaling in hematopoietic cells is required for the generation of Ly6Chi monocytes. Of note&s_comma; WT BM reconstituted Ifnar1-/- chimeric mice with increased numbers of Ly6Chi monocytes and decreased numbers of neutrophils survived longer than influenza-infected Ifnar1-/- mice. In contrast&s_comma; WT mice that received Ifnar1-/- BM cells with alternative Ly6Cint monocytes and increased numbers of neutrophils exhibited higher mortality rates than WT mice given WT BM cells. Collectively&s_comma; these data suggest that IFN-I contributes to resistance of influenza infection by control of monocytes and neutrophils in the lung.

Host: Hiroshi Kiyono (Division of Mucosal Immunology )&s_comma;

Sumiko Watanabe (Division of Molecular and Development Biology )