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1+ 
T Cells Control Early Infiltration of Neutrophils after Escherichia coli Infection via IL-17 Production1
* Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan;
Department of Biomolecular Sciences, Faculty of Medicine, Saga University, Saga, Japan; and
Department of Immunology and Parasitology, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan
Neutrophils infiltrate the site of infection and play critical roles in host defense, especially against extracellular bacteria. In the present study, we found a rapid and transient production of IL-17 after i.p. infection with Escherichia coli, preceding the influx of neutrophils. Neutralization of IL-17 resulted in a reduced infiltration of neutrophils and an impaired bacterial clearance. Ex vivo intracellular cytokine flow cytometric analysis revealed that 
T cell population was the major source of IL-17. Mice depleted of T cells by mAb treatment or mice genetically lacking V1 showed diminished IL-17 production and reduced neutrophil infiltration after E. coli infection, indicating an importance of V1+ T cells as the source of IL-17. It was further revealed that T cells in the peritoneal cavity of naive mice produced IL-17 in response to IL-23, which was induced rapidly after E. coli infection in a TLR4 signaling-dependent manner. Thus, although T cells are generally regarded as a part of early induced immune responses, which bridge innate and adaptive immune responses, our study demonstrated a novel role of T cells as a first line of host defense controlling neutrophil-mediated innate immune responses.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by the Program of Founding Research Centers for Emerging and Reemerging Infectious Diseases, which was launched as a project commissioned by the Ministry of Education, Culture, Sports, Science, and Technology, Japan; by Grant-in-Aid for Japan Society for Promotion of Science; and by grants from the Japanese Ministry of Education, Science, and Culture (to Y.Y.).
2 Address correspondence and reprint requests to Dr. Hisakata Yamada, Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. E-mail address: hisakata{at}bioreg.kyushu-u.ac.jp
3 Abbreviations used in this paper: PEC, peritoneal exudate cell; Ct, cycle threshold; mIL, murine IL.
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