International Immunology, Vol. 15, No. 2, pp. 251-260,
February 2003
© 2003 Japanese Society for Immunology
IL-1-induced tumor necrosis factor-
elicits inflammatory cell infiltration in the skin by inducing IFN-
-inducible protein 10 in the elicitation phase of the contact hypersensitivity response
1 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan 2 Department of Molecular Preventive Medicine, School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113 0033, Japan 3 Department of Immunology, National Institute of Animal Health, 3-1-1 Kannonndai, Tsukuba City 305-0856, Japan 4 Present address: Institute of Experimental Animals, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano 390-8621, Japan 5 Present address: Institute for Experimental Animals, School of Medicine, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-8640, Japan
Correspondence to: Y. Iwakura; E-mail: iwakura{at}ims.u-tokyo.ac.jp
Transmitting editor: K. Sugamura
Contact hypersensitivity (CHS) is a typical inflammatory response against contact allergens. Inflammatory cytokines, including IL-1 and tumor necrosis factor (TNF)-
, are implicated in the reaction, although the precise roles of each cytokine have not been completely elucidated. In this report, we dissected the functional roles of IL-1 and TNF- during CHS. CHS induced by 2,4,6-trinitorochlorobenzene as well as oxazolone was suppressed in both IL-1/ß–/– and TNF-–/– mice. Hapten-specific T cell activation, as examined by T cell proliferation, OX40 expression and IL-17 production, was reduced in IL-1/ß–/– mice, but not in TNF-–/– mice, suggesting that IL-1 but not TNF- is required for hapten-specific T cell priming in the sensitization phase. On the other hand, TNF-, induced by IL-1, was necessary for the induction of local inflammation during the elicitation phase. We also found that the expression of IFN-
-inducible protein 10 (IP-10) was augmented at the inflammatory site. Although IP-10 mRNA expression was abrogated in TNF-–/– mice, both CHS development and TNF- mRNA expression occurred normally in IFN-–/– mice, indicating that the induction of IP-10 during CHS was primarily controlled by TNF-. Interestingly, CHS was suppressed by treatment with anti-IP-10 mAb, suggesting a critical role for IP-10 in CHS. Reduced CHS in TNF-–/– mice was reversed by IP-10 injection during the elicitation phase. Thus, it was shown that the roles for IL-1 and TNF- are different, although both cytokines are crucial for the development of CHS.
Keywords: chemokine, contact hypersensitivity, cytokine, knockout mice
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