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The Journal of Immunology, 2006, 177: 4276-4280.
Copyright © 2006 by The American Association of Immunologists, Inc.


CUTTING EDGE

Cutting Edge: Uniqueness of Lymphoid Chemokine Requirement for the Initiation and Maturation of Nasopharynx-Associated Lymphoid Tissue Organogenesis1

Satoshi Fukuyama*, Takahiro Nagatake*, Dong-Young Kim*, Kaoru Takamura*, Eun Jeong Park*, Tsuneyasu Kaisho{dagger}, Norimitsu Tanaka{ddagger}, Yuichi Kurono{ddagger} and Hiroshi Kiyono2,*

* Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan; {dagger} RIKEN Research Center for Allergy and Immunology, Yokohama, Japan; and {ddagger} Department of Otolaryngology, Head and Neck Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan

CD3CD4+CD45+ inducer cells are required for the initiation of mucosa-associated organogenesis of both nasopharynx-associated lymphoid tissues (NALT) and Peyer’s patches (PP) in the aerodigestive tract. CXCL13–/– mice and mice carrying the paucity of lymph node T cell (plt) mutation and lacking expression of CCL19 and CCL21 accumulate CD3CD4+CD45+ cells at the site of NALT but not of PP genesis. Although NALT was observed to develop in adult CXCL13–/– and plt/plt mice, the formation of germinal centers in CXCL13–/– mice was affected, and their population of B cells was much lower than in the NALT of CXCL13+/– mice. Similarly, fewer T cells were observed in the NALT of plt/plt mice than in control mice. These findings indicate that the initiation of NALT organogenesis is independent of CXCL13, CCL19, and CCL21. However, the expression of these lymphoid chemokines is essential for the maturation of NALT microarchitecture.

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 Core Research for Evolutional Science and Technology Program, from Japan Science and Technology Corporation, and a Grant-in-Aid from the Ministry of Education, Science, Sports, and Culture and the Ministry of Health and Welfare of Japan. S.F. was supported by research fellowships from the Japan Society for the Promotion of Science for Young Scientists. D.-Y.K. was supported by research fellowships from the Japan Society for the Promotion of Science for Foreign Researchers.

2 Address correspondence and reprint requests to Dr. Hiroshi Kiyono, Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. E-mail address: kiyono{at}ims.u-tokyo.ac.jp

3 Abbreviations used in this paper: NALT, nasopharynx-associated lymphoid tissue; PP, Peyer’s patch; LT, lymphotoxin; LN, lymph node; E17, 17-day-old embryo; LDM, laser microdissection; FDC, follicular dendritic cell; PNA, peanut agglutinin; NALTi, NALT inducer cell; PPi, PP inducer cell; MLN, mesenteric LN.




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