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Identification of CD25⁺ T Cells As Fetal Thymus-Derived Naturally Occurring IL-17 Producers¹

Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan

We previously reported that resident T cells in the peritoneal cavity rapidly produced IL-17 in response to Escherichia coli infection to mobilize neutrophils. We found in this study that the IL-17-producing T cells did not produce IFN- or IL-4, similar to Th17 cells. IL-17-producing T cells specifically express CD25 but not CD122, whereas CD122⁺ T cells produced IFN-. IL-17-producing T cells were decreased but still present in IL-2- or CD25-deficient mice, suggesting a role of IL-2 for their maintenance. IFN--producing CD122⁺ T cells were selectively decreased in IL-15-deficient mice. Surprisingly, IL-17-producing T cells were already detected in the thymus, although CD25 was not expressed on the intrathymic IL-17-producing T cells. The number of thymic IL-17-producing T cells was peaked at perinatal period and decreased thereafter, coincided with the developmental kinetics of V6⁺V1⁺ T cells. The number of IL-17-producing T cells was decreased in fetal thymus of V1-deficient mice, whereas V5⁺ fetal thymocytes in normal mice did not produce IL-17. Thus, it was revealed that the fetal thymus-derived V6⁺V1⁺ T cells functionally differentiate to produce IL-17 within thymus and thereafter express CD25 to be maintained in the periphery.

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 a 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. and H.Y.). K.S. is supported by a Postdoctoral Fellowship from the Japan Society for the Promotion of Science.

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; Treg, regulatory T cell; ED, embryonic development.

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