短期紫外线照射对接触性超敏反应的抑制作用：II. 尿刊酸的作用。
Suppression of contact hypersensitivity by short-term ultraviolet irradiation: II. The role of urocanic acid.
作者信息
Harriott-Smith T G, Halliday W J
机构信息
Microbiology Department, University of Queensland, St Lucia, Australia.
出版信息
Clin Exp Immunol. 1988 Apr;72(1):174-7.
Cis-urocanic acid (cis-UCA), produced from trans-UCA (a normal component of epidermis) by UV irradiation, suppressed cell-mediated immunological reactions in vivo and in vitro. It suppressed the development of contact hypersensitivity (CHS) when injected into mice, and it suppressed leucocyte adherence inhibition (LAI) reactions of previously sensitized lymphocytes exposed to antigen. Serum from mice injected with cis-UCA was also immunosuppressive in vitro. Normal murine spleen cells cultured with cis-UCA produced a non-dialysable factor which suppressed LAI reactivity. Trans-UCA was ineffectual in all of these systems. Both the ability of cis-UCA to induce an immunosuppressive serum factor and its ability to suppress CHS were abrogated by prior administration of cyclophosphamide, indicating that cis-UCA (normally from irradiated epidermis) stimulates T suppressor cells to produce the previously described suppressor factor in serum and the immunosuppression associated with short-term irradiation.
顺式尿刊酸（cis-UCA）由反式尿刊酸（表皮的一种正常成分）经紫外线照射产生，在体内和体外均能抑制细胞介导的免疫反应。将其注射到小鼠体内时，可抑制接触性超敏反应（CHS）的发生，并且能抑制先前致敏的淋巴细胞暴露于抗原时的白细胞黏附抑制（LAI）反应。注射了顺式尿刊酸的小鼠血清在体外也具有免疫抑制作用。用顺式尿刊酸培养的正常小鼠脾细胞产生了一种不可透析的因子，该因子可抑制LAI反应性。反式尿刊酸在所有这些系统中均无效。预先给予环磷酰胺可消除顺式尿刊酸诱导免疫抑制血清因子的能力及其抑制CHS的能力，这表明顺式尿刊酸（通常来自受照射的表皮）刺激T抑制细胞产生血清中先前描述的抑制因子以及与短期照射相关的免疫抑制作用。
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