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Blood, 1 May 2007, Vol. 109, No. 9, pp. 3640-3648. Prepublished online as a Blood First Edition Paper on December 29, 2006; DOI 10.1182/blood-2006-09-046128. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2006-09-046128v1 109/9/3640    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Nakae, S. Articles by Galli, S. J. Search for Related Content PubMed PubMed Citation Articles by Nakae, S. Articles by Galli, S. J. Related Collections Phagocytes Cell Cycle Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS Mast cell–derived TNF can promote Th17 cell–dependent neutrophil recruitment in ovalbumin-challenged OTII mice Susumu Nakae1, Hajime Suto1,2, Gerald J. Berry1, and Stephen J. Galli1 1 Department of Pathology, Stanford University School of Medicine, Stanford, CA; 2 Atopy Research Center, Juntendo University, Tokyo, Japan Both mast cells and IL-17 can contribute to host defense and pathology in part by orchestrating neutrophil recruitment, but the possible role of mast cells in IL-17–induced inflammation remains to be defined. We found that mast cells and IL-17, but neither IFN- nor FcR signaling, contributed significantly to the antigen (Ag)–dependent airway neutrophilia elicited in ovalbumin-specific T-cell receptor (TCR)–expressing C57BL/6-OTII mice, and that IFN- significantly suppressed IL-17–dependent airway neutrophilia in this setting. IL-18, IL-1ß, and TNF each contributed significantly to the development of Ag- and T helper 17 (Th17 cell)–mediated airway neutrophilia. Moreover, IL-17 enhanced mast cell TNF production in vitro, and mast cell–associated TNF contributed significantly to Ag- and Th17 cell–mediated airway neutrophilia in vivo. By contrast, we detected no significant role for the candidate mediators histamine, PGD2, LTB4, CXCL10, or IL-16, each of which can be produced by mast cells and other cell types, in the neutrophil infiltration elicited in this model. These findings establish that mast cells and mast cell–derived TNF can significantly enhance, by FcR-independent mechanisms, the Ag- and Th17 cell–dependent development of a neutrophil-rich inflammatory response at a site of Ag challenge. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Ding, J. G. Nedrud, B. Wershil, R. W. Redline, T. G. Blanchard, and S. J. Czinn Partial Protection against Helicobacter pylori in the Absence of Mast Cells in Mice Infect. Immun., December 1, 2009; 77(12): 5543 - 5550. [Abstract] [Full Text] [PDF] S. Tanaka, T. Yoshimoto, T. Naka, S. Nakae, Y.-i. Iwakura, D. Cua, and M. Kubo Natural Occurring IL-17 Producing T Cells Regulate the Initial Phase of Neutrophil Mediated Airway Responses J. Immunol., December 1, 2009; 183(11): 7523 - 7530. [Abstract] [Full Text] [PDF] I. Waern, S. Jonasson, J. Hjoberg, A. Bucht, M. Abrink, G. Pejler, and S. 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