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在小鼠抗人异种混合淋巴细胞反应中,针对人类MHC产物的小鼠T淋巴细胞增殖反应。

Mouse T lymphocytes proliferative responses specific for human MHC products in mouse anti-human xenogeneic MLR.

作者信息

Yoshizawa K, Yano A

出版信息

J Immunol. 1984 Jun;132(6):2820-9.

PMID:6202762
Abstract

It has been reported that human T cells recognize the polymorphism of murine Ia antigens in the human anti-mouse xenogeneic mixed lymphocyte reactions (MLR). In this study, murine T cell recognition of human Class II antigens of the major histocompatibility complex (MHC) was analyzed in mouse anti-human xenogeneic MLR responses. The xenoreactive murine T cell proliferative response was blocked by adding anti-HLA-DR monoclonal antibody to the xenogeneic MLR culture. The specificity of xenoreactive murine T cells was examined with regard to the secondary and tertiary xenogeneic MLR system. The xenoreactive murine T cells were restimulated by distinct human stimulator cells that had no shared HLA antigens with the stimulator used in the primary MLR. The data presented here show that the murine xenoreactive T cells recognize the shared determinant(s) of HLA-DR antigen on non-T, non-B stimulator cells. The xenoreactive murine T cell proliferative responses were mediated by Thy-1+, Lyt-1+, and Lyt-2- cells. Furthermore, the xenoreactive T cell responses required Ia+ cells, and Ia antigen on accessory cells plays a crucial role in eliciting the xenoreactive responses against human stimulator cells, while Ia+ accessory cells in the responding cell population are not essential for the elicitation of allogeneic MLR responses, as reported previously.

摘要

据报道,在人类抗小鼠异种混合淋巴细胞反应(MLR)中,人类T细胞可识别小鼠Ia抗原的多态性。在本研究中,在小鼠抗人类异种MLR反应中分析了小鼠T细胞对人类主要组织相容性复合体(MHC)II类抗原的识别。通过向异种MLR培养物中添加抗HLA-DR单克隆抗体,阻断了异种反应性小鼠T细胞的增殖反应。在二级和三级异种MLR系统中检测了异种反应性小鼠T细胞的特异性。用与初次MLR中使用的刺激细胞没有共同HLA抗原的不同人类刺激细胞重新刺激异种反应性小鼠T细胞。此处给出的数据表明,小鼠异种反应性T细胞识别非T、非B刺激细胞上HLA-DR抗原的共同决定簇。异种反应性小鼠T细胞的增殖反应由Thy-1+、Lyt-1+和Lyt-2-细胞介导。此外,异种反应性T细胞反应需要Ia+细胞,辅助细胞上的Ia抗原在引发针对人类刺激细胞的异种反应中起关键作用,而如先前报道,反应细胞群体中的Ia+辅助细胞对于同种异体MLR反应的引发并非必不可少。

相似文献

1
Mouse T lymphocytes proliferative responses specific for human MHC products in mouse anti-human xenogeneic MLR.在小鼠抗人异种混合淋巴细胞反应中,针对人类MHC产物的小鼠T淋巴细胞增殖反应。
J Immunol. 1984 Jun;132(6):2820-9.
2
Requirement of Ia-positive accessory cells in the MLR response against class II antigen on human B cell tumor line.在针对人B细胞肿瘤系上II类抗原的混合淋巴细胞反应中Ia阳性辅助细胞的需求。
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The immunobiology of T cell responses to Mls-locus-disparate stimulator cells. II. Effects of Mls-locus-disparate stimulator cells on cloned, protein antigen-specific, Ia-restricted T cell lines.T细胞对Mls位点不同的刺激细胞反应的免疫生物学。II. Mls位点不同的刺激细胞对克隆的、蛋白质抗原特异性、Ia限制的T细胞系的影响。
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Xenogeneic cells and superantigen induce human T-cell activation in the absence of T-cell recognition of xenoantigen.异种细胞和超抗原在T细胞不识别异种抗原的情况下诱导人T细胞活化。
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Activation of human T lymphocyte subsets: helper and suppressor/cytotoxic T cells recognize and respond to distinct histocompatibility antigens.人类T淋巴细胞亚群的激活:辅助性T细胞和抑制性/细胞毒性T细胞识别并对不同的组织相容性抗原作出反应。
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Search for class II major histocompatibility complex molecular involvement in the response of Lyt-2+ cytotoxic T lymphocyte precursors to alloantigen.寻找II类主要组织相容性复合体分子在Lyt-2+细胞毒性T淋巴细胞前体对同种异体抗原反应中的作用。
Eur J Immunol. 1985 Nov;15(11):1125-30. doi: 10.1002/eji.1830151111.

引用本文的文献

1
Human CD4 restores normal T cell development and function in mice deficient in murine CD4.人类CD4可恢复缺乏鼠源CD4的小鼠的正常T细胞发育和功能。
J Exp Med. 1994 Apr 1;179(4):1233-42. doi: 10.1084/jem.179.4.1233.
2
Xenogeneic proliferation and lymphokine production are dependent on CD4+ helper T cells and self antigen-presenting cells in the mouse.在小鼠中,异种增殖和淋巴因子产生依赖于CD4 +辅助性T细胞和自身抗原呈递细胞。
J Exp Med. 1990 Aug 1;172(2):567-75. doi: 10.1084/jem.172.2.567.
3
Species specificity and augmentation of responses to class II major histocompatibility complex molecules in human CD4 transgenic mice.
人类CD4转基因小鼠中对II类主要组织相容性复合体分子反应的物种特异性及增强作用。
J Exp Med. 1992 Jun 1;175(6):1707-15. doi: 10.1084/jem.175.6.1707.
4
Different recognition of transgenic HLA-DQw6 molecules by mouse CD4+ and CD8+ T cells.小鼠CD4+和CD8+ T细胞对转基因HLA-DQw6分子的不同识别。
Immunogenetics. 1992;35(1):46-50. doi: 10.1007/BF00216626.