Studies on Iuduction of Autologous MLR in the Autoimmune Diseases and its Pathological Roles.
Studies on Iuduction of Autologous MLR in the Autoimmune Diseases and its Pathological Roles.
批准号:
01480186
负责人:
KUMAGAI Katsuo
金额:
$0.83万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (B)
财政年份:
1989
资助国家:
日本
项目状态:
已结题
起止时间:
1989 至 1990
中文摘要
关于自体混合淋巴细胞反应(MLR)的特异性及其生物学意义,得到以下结果:(1)用刺激细胞和应答淋巴细胞混合的神经氨酸酶治疗可显著增强自体MLR中的DNA复制。(2)利用该方法,我们能够证明自体MLR是DR抗原诱导的辅助性T (TH)激活辅助细胞(AC),其DNA复制不依赖于il -2,但依赖于多种细胞因子,IL-3, IL-5, IL-6和IL-7。(3)自体MLR也被发现诱导产生活化的CD4^+辅助性T细胞,以及CD4^- cd8 ^-双阴性(DN) T细胞,其表型为alphabetaT细胞受体(alphabetaTcR)^+或gammadeltaTcR^+。(4)基于所发现的自体MLR的特异性,淋巴细胞增殖。分析了MRL/lpr小鼠淋巴组织的诱导作用。结果发现,淋巴组织中CD3^+CD4^-CD8^-B220^+ alphabetaTcR^+T细胞的异常增殖可能是一种现象,该群体的前体可以通过表面的某些抗原介导,对自体辅助细胞作出反应而增殖。
英文摘要
On the specific nature and its biological significance of autologous mixed lymphocyte reaction (MLR), the following results are obtained. (1) Treatment with neuraminidase of the mixtures of stimulator cells and responder lymphocytes results in a marked enhancement of DNA replication in the autologous MLR. (2) Using this method, we are able to demonstrate that the autologous MLR is a helper T (TH) activation induced by DR antigens on accessory (AC) cells, of which the DNA replication is IL-2-independent, but dependent upon the multiple cytokines, IL-3, IL-5, IL-6 and IL-7. (3) The autologous MLR is also found to induce the generation of activated CD4^+ helper T cells, and also CD4^-CD8^- double negative (DN) T cells with a phenotype of alphabetaT cell receptor (alphabetaTcR)^+ or gammadeltaTcR^+. (4) Based on the findings of the specific nature of autologous MLR, the lymphoproliferation. Induced in the lymphoid tissues of MRL/lpr mouse is analyzed. As a result, it is found that abnormal proliferation of CD3^+CD4^-CD8^-B220^+ alphabetaTcR^+T cells in the lymphoid tissues may be a phenomenon in which precursors for this population can be proliferated in response to autologous accessory cells, mediated through certain antigens on the surface.
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SHUHJI SEKI: "Identification of activated T cell receptor gamma delta lymphocytes in the liver of tumorーbearing hosts." J.Clin.Invest.86. 409-415 (1990)
SHUHJI SEKI:“荷瘤宿主肝脏中活化 T 细胞受体 γ δ 淋巴细胞的鉴定。”J.Clin.Invest.86 (1990)。
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MASATO KATO: "Responses of pokeweed mitogenーstimulated peripheral mononuclear cells to human recombinant interleukins 3 and 4." Lymphokine Res.9. 247-255 (1990)
加藤正人:“美洲商陆促细胞分裂原刺激的外周单核细胞对人重组白细胞介素 3 和 4 的反应。” 247-255 (1990)。
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Kumagai,K.: "Production of interleukin 1 inhibitors by the murine macrophage cell line P388D_1 which produces interleukin 1" Immunol.Microbiol.33. 43-57 (1989)
Kumagai,K.:“产生白细胞介素 1 的鼠巨噬细胞系 P388D_1 产生白细胞介素 1 抑制剂”Immunol.Microbiol.33。
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Ohteki, T., Seki, S., Abo, T., and Kumagai, K.: "Liver is a possible site for the proliferation of abnormal CD3^+4^-8^- double-negative lymphocytes in autoimmune MRL-lpr/lpr mice." J. Exd. Med.172. 7-12 (1990)
Ohteki, T.、Seki, S.、Abo, T. 和 Kumagai, K.:“肝脏是自身免疫 MRL-lpr/ 中异常 CD3^ 4^-8^- 双阴性淋巴细胞增殖的可能部位
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Kumagai,K.: "Polyclonal activation of human lymphocytes by streptococcal preparations.Evidence for interlekin 2-independent generation of “double negative (CD3^+CD4^-CD8^-TcRγ/δ^+)"T.cells." J.Immunol.(1990)
Kumagai, K.:“链球菌制剂对人类淋巴细胞的多克隆激活。“双阴性 (CD3^+CD4^-CD8^-TcRγ/δ^+)”T 细胞独立于 interlekin 2 生成的证据。”免疫学(1990)
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共 21 条
Unusual increase of extrathymic T cells in the liver of autoimmune MRL-1pr/1pr mice.
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批准号:05454202
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项目类别:Grant-in-Aid for General Scientific Research (B)
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资助金额:$3.01万
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财政年份:1993
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负责人:KUMAGAI Katsuo
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依托单位:
海外基金