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作 者:司秋生[1] 郑秀娟[1] 金帆[1] 林云璐[1] 何球藻[1]
机构地区:[1]上海医科大学免疫学教研室
出 处:《免疫学杂志》1993年第3期171-174,共4页Immunological Journal
摘 要:本文采用H22小鼠肝癌模型研究了带瘤小鼠淋巴细胞IL-2R表达的改变,结果表明:IL-2R表达随肿瘤生长而逐渐减少,且前列腺素E、肿瘤性免疫抑制因子和抑制性T淋巴细胞对IL-2R的表达都具有抑制作用。这一研究对于阐明带瘤宿主细胞免疫功能低下的机理具有重要意义。The present study was performed to elucidate the relationship between the H22 hepatoma growth and the decreased ability of mouse spleen cells to secrete Interleukin-2 (IL-2) and to express IL-2 receptor(IL-2R).The results showed that the spleen cells from tumor-bearing mouse(TBM) produce less IL-2 than those of their normal counterparts. However, addition of exogenous IL-2 only partially improved the impaired concanavalin A(ConA) responsiveness of lymphocytes of the TBM. The absorption investigation indicated that the ConA-activated spleen cells from the TBM were less receptive to IL-2,which suggested the defect of IL--2R expression. We therefore analyzed the percentage of IL-2R positive cells. The results demonstrated that the number of lymphocytes induced to express IL-2R decreases with increasing tumor burden. The further study indicated that the prostaglandine ( immunosuppressive factors secreted by H22 hepatoma cells and the suppressor T lymphocytes inhibite the lymphocytes to express IL-2R in TBM. Our data suggested that the reduced ability to secret IL-2 and to express IL-2R may be one of the reasons for the impaired cell-mediated immune response in tumor bearing host.
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