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V1⁺ T Cells Producing CC Chemokines May Bridge a Gap between Neutrophils and Macrophages in Innate Immunity during Escherichia coli Infection in Mice¹

Tetsuzo Tagawa^*,, Hitoshi Nishimura^2,*, Toshiki Yajima^*, Hiromitsu Hara^*, Kenji Kishihara^*, Goro Matsuzaki, Ichiro Yoshino, Yoshihiko Maehara and Yasunobu Yoshikai^*

^* Division of Host Defense, Research Center for Prevention of Infectious Diseases, Medical Institute of Bioregulation, and Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; and Division of Molecular Microbiology, University of Ryukyus Center of Molecular Biosciences, Okinawa, Japan

An influx of neutrophils followed a short time later by an influx of macrophages to the infected site plays a key role in innate immunity against Escherichia coli infection. We found in this study that V1^–/– mice exhibited impaired accumulation of peritoneal macrophages but not neutrophils and delayed bacterial clearance after i.p. inoculation with E. coli. Peritoneal T cells from E. coli-infected wild-type mice produced CCL3/MIP-1 and CCL5/RANTES in response to TCR triggering in vitro, whereas such production was not evident in T cells from E. coli-infected V1^–/– mice. Neutralization of CCL3/MIP-1 by a specific mAb in vivo significantly inhibited the accumulation of macrophages in the peritoneal cavity after E. coli infection, resulting in exacerbated bacterial growth in the peritoneal cavity. These results suggest that V1⁺ T cells bridge a gap between neutrophils and macrophages in innate immunity during E. coli infection mediated by production of CC chemokines, enhancing macrophage trafficking to the site of infection.

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The JI 2004 173: 4763-4764. [Full Text]  

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