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用二甲基亚砜处理后,H-2抗原缺陷型小鼠肺癌细胞的免疫识别增强。

Enhanced immune recognition of H-2 antigen-deficient murine lung carcinoma cells following treatment with dimethyl sulfoxide.

作者信息

Bahler D W, Lord E M

出版信息

Cancer Res. 1985 Dec;45(12 Pt 1):6362-5.

PMID:3877567
Abstract

Dimethyl sulfoxide (DMSO) has previously been shown to increase the surface expression of H-2K and H-2D antigens on cultured line 1 carcinoma cells. H-2 densities increase from initial levels barely detectable with flow cytometry to those found on normal BALB/c spleen cells. Here we compare the susceptibilities of untreated and DMSO-treated line 1 cells to lysis mediated by H-2d specific monoclonal antibodies and complement, cytotoxic T-cells, and natural killer cells. Induced H-2 antigens appear to function normally in that DMSO-treated cells are highly susceptible to all types of H-2 restricted immune lysis, whereas untreated line 1 cells are not. DMSO does not increase lysis of line 1 cells mediated by natural killer cells. Our results suggest that DMSO could be used to make the growth of major histocompatibility complex antigen-deficient tumors more sensitive to T-cell-mediated immunological resistance.

摘要

二甲基亚砜(DMSO)先前已被证明可增加培养的1号线癌细胞上H-2K和H-2D抗原的表面表达。H-2密度从最初用流式细胞术几乎检测不到的水平增加到正常BALB/c脾细胞上发现的水平。在这里,我们比较了未处理和DMSO处理的1号线细胞对由H-2d特异性单克隆抗体和补体、细胞毒性T细胞和自然杀伤细胞介导的裂解的敏感性。诱导的H-2抗原似乎功能正常,因为DMSO处理的细胞对所有类型的H-2限制性免疫裂解高度敏感,而未处理的1号线细胞则不然。DMSO不会增加自然杀伤细胞介导的1号线细胞的裂解。我们的结果表明,DMSO可用于使主要组织相容性复合体抗原缺陷肿瘤的生长对T细胞介导的免疫抗性更敏感。

相似文献

1
Enhanced immune recognition of H-2 antigen-deficient murine lung carcinoma cells following treatment with dimethyl sulfoxide.用二甲基亚砜处理后,H-2抗原缺陷型小鼠肺癌细胞的免疫识别增强。
Cancer Res. 1985 Dec;45(12 Pt 1):6362-5.
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Dimethyl sulfoxide induces expression of H-2 antigens on mouse lung carcinoma cells.
J Immunol. 1985 Apr;134(4):2790-8.
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Lysis of a lung carcinoma by poly I:C-induced natural killer cells is independent of the expression of class I histocompatibility antigens.
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Molecular analysis of deficient class I H-2 antigen expression by mouse lung carcinoma cells.
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Mechanism of cytolytic T lymphocyte killing of a low class I-expressing tumor.细胞毒性T淋巴细胞杀伤低表达I类分子肿瘤的机制
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Macrophage-mediated natural cytotoxicity of dimethyl sulfoxide-treated Friend erythroleukemia cells.巨噬细胞介导的二甲基亚砜处理的弗氏红白血病细胞的天然细胞毒性。
J Natl Cancer Inst. 1985 Jul;75(1):105-10.
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T lymphocyte responses to multiple minor histocompatibility antigens generate both self-major histocompatibility complex-restricted and cross-reactive cytotoxic T lymphocytes.T淋巴细胞对多种次要组织相容性抗原的反应会产生自身主要组织相容性复合体限制的和交叉反应性细胞毒性T淋巴细胞。
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Alloreactivity and tumor antigens: generation of syngeneic antilymphoma killer lymphocytes by alloimmunization of mice with normal cells.同种异体反应性与肿瘤抗原:通过用正常细胞对小鼠进行同种异体免疫来产生同基因抗淋巴瘤杀伤淋巴细胞。
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Cross-reacting antigens on L5178Y cells which serve as targets for cytotoxic T-lymphocyte lysis during establishment of the tumor dormant state.L5178Y细胞上的交叉反应抗原,在肿瘤休眠状态建立过程中作为细胞毒性T淋巴细胞裂解的靶标。
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