Impaired contact hypersensitivity in macrophage migration inhibitory factor-deficient mice |
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Authors: | Shimizu Tadamichi Abe Riichiro Nishihira Jun Shibaki Akihiko Watanabe Hirokazu Nakayama Toshinori Taniguchi Masaru Ishibashi Teruo Shimizu Hiroshi |
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Institution: | Department of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan. |
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Abstract: | To determine whether macrophage migration inhibitory factor (MIF) is required for contact hypersensitivity (CHS) response, MIF-deficient (MIF KO) and wild-type (WT) mice were sensitized with trinitrochlorobenzene (TNCB) or oxazolone on their abdominal skin and challenged on the dorsum skin of one ear 5 days later. Significant ear swelling was observed in the WT mice, but this response was inhibited in the MIF KO mice (p<0.01 for MIF KO vs. WT mice in 24 h). In addition, lymph node cells from hapten-sensitized MIF KO mice showed a decreased capacity for transferring the CHS response. A topical application of TNCB (200 microg) caused a significant decline in epidermal Langerhans cell (LC) density (20.3%; p<0.01 compared with vehicle) 4 h after application in WT mice, but it failed to provoke a significant epidermal LC migration in MIF KO mice (7.4%). By mixed lymphocyte reaction, the T cell proliferative response to alloantigen was significantly decreased in the MIF KO mice compared with WT mice (p<0.005). Taken together, these results indicate that MIF is pivotal in the regulation of cutaneous immune responses and plays a central role in LC migration and T cell proliferation for the CHS response. |
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Keywords: | Contact hypersensitivity Delayed‐type hypersensitivity Macrophage migration inhibitory factor |
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