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International Immunology, Vol. 13, No. 12, 1471-1478, December 2001
© 2001 Japanese Society for Immunology

IL-1{alpha}, but not IL-1ß, is required for contact-allergen-specific T cell activation during the sensitization phase in contact hypersensitivity

Susumu Nakae, Chie Naruse-Nakajima11, Katsuko Sudo, Reiko Horai, Masahide Asano1 and Yoichiro Iwakura

Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
1 Present address: Institute for Experimental Animals, School of Medicine, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-8640, Japan

Correspondence to: Y. Iwakura

Contact hypersensitivity (CHS) is a T cell-mediated cellular immune response caused by epicutaneous exposure to contact allergens. In this reaction, after the first epicutaneous allergen sensitization, Langerhans cells (LC) catch allergens and migrate from the skin to draining lymph nodes (LN) and activate naive T cells. Although IL-1 is suggested to be involved in these processes, the mechanisms have not been elucidated completely. In this report, to elucidate roles of IL-1{alpha} and IL-1ß in CHS, we analyzed ear swelling in 2,4,6-trinitrochlorobenzene (TNCB)-induced CHS using gene-targeted mice. We found that ear swelling was suppressed in IL-1{alpha}-deficient (IL-1{alpha}–/–) mice but not in IL-1ß–/– mice. LC migration from the skin into LN was delayed in both IL-1{alpha}–/– and IL-1ß–/– mice, suggesting that this defect was not the direct cause for the reduced CHS in these mice. However, we found that the proliferative response of trinitrophenyl (TNP)-specific T cells after sensitization with TNCB was specifically reduced in IL-1{alpha}–/– mice. Furthermore, adoptive transfer of TNP-conjugated IL-1-deficient epidermal cells (EC) into wild-type mice indicated that only IL-1{alpha}, but not IL-1ß, produced by antigen-presenting cells in EC could prime allergen-specific T cells. These observations indicate that IL-1{alpha}, but not IL-1ß, plays a crucial role in TNCB-induced CHS by sensitizing TNP-specific T cells.

Keywords: contact hypersensitivity, IL-1, knockout mice, Langerhans cell

Transmitting editor: K.Sugamura


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