Suppression of mouse contact hypersensitivity after treatment with antibodies to leukocyte function-associated antigen-1 and intercellular adhesion molecule-1

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作者
M. Murayama
H. Yasuda
Y. Nishimura
M. Asahi
机构
[1] Department of Dermatology,
[2] University of Occupational and Environmental Health,undefined
[3] 1-1Iseigaoka,undefined
[4] Yahata-Nishi-Ku,undefined
[5] Kitakyushu,undefined
[6] Japan,undefined
[7] Department of Clinical Immunology,undefined
[8] University of Occupational and Environmental Health,undefined
[9] 1-1 Iseigaoka,undefined
[10] Yahata-Nishi-Ku,undefined
[11] Kitakyushu,undefined
[12] Japan,undefined
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关键词
Key words Contact hypersensitivity; Dinitrofluorobenzene; Cell adhesion molecule; LFA-1/ICAM-1 interaction; Interleukin 2;
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摘要
We investigated the effects of the antibodies against the adhesion molecules leucocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) on mouse allergic contact hypersensitivity. Mice were injected intraperitoneally with both antibodies before sensitization by an epicutaneous application of dinitrofluorobenzene (DNFB). Simultaneous administration of the antibodies induced suppression of ear swelling in the effector phase of contact hypersensitivity. To show the effect of antibodies in vitro, lymph node cells (LNC) of mice treated with antibodies or with phosphate-buffered saline (PBS) were cultured in the presence of dinitrobenzene sulphonic sodium salts (DNBS), and the production of interleukin-2, interleukin-4 and interleukin-10 in the culture supernatants was measured using an enzyme-linked immunosorbent assay (ELISA). It was found that the production of interleukin-2 in the cells of mice treated with the antibodies was significantly lower than in the cells of PBS-treated mice. On the other hand, no difference was noted in the production of interleukin-4 or interleukin-10. Our results indicate that in vivo simultaneous administration of antibodies to cell adhesion molecules before hapten sensitization induces the suppression of contact hypersensitivity in mice and that the suppression may be due to the inhibition of the production of interleukin-2.
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页码:98 / 103
页数:5
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