ACTIVATION OF HUMAN LYMPHOCYTES-T .1. REQUIREMENTS FOR MITOGEN-INDUCED PROLIFERATION OF ANTIGEN-SPECIFIC LYMPHOCYTE-T CLONES
ACTIVATION OF HUMAN LYMPHOCYTES-T .1. REQUIREMENTS FOR MITOGEN-INDUCED PROLIFERATION OF ANTIGEN-SPECIFIC LYMPHOCYTE-T CLONES
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DOI：
10.1002/eji.1830131204
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发表时间：
1983-01-01
影响因子：
5.4
通讯作者：
FLEISCHER, B
中科院分区：
文献类型：
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作者：
FLEISCHER, B
在辅助细胞（AC）依赖性丝裂原诱导的T细胞增殖模型系统中，研究了几种人类抗原特异性、hla限制性辅助性T淋巴细胞克隆（HTLC）对丝裂原[豆豆蛋白a、植物血凝素、葡萄球菌蛋白a、美洲商陆丝裂原]的反应。HTLC本身对各种有丝分裂原或半乳糖氧化酶的氧化没有或只有微弱的反应，但如果将某些肿瘤细胞系作为AC加入到实验中，反应可能会强烈增强。用凝集素预处理或HTLC或AC的氧化都能有效地刺激该系统中T细胞的增殖。氧化过程中形成的醛的减少完全消除了氧化B淋巴母细胞样细胞系的刺激活性。这表明T细胞和AC的交联是诱导增殖所必需的。当测试几种已建立的细胞系在该系统中作为AC功能的能力时，检测到AC活性的深刻差异。AC活性差的细胞不能刺激HTLC并非由于一些微不足道的原因，例如需要不同的有丝分裂原浓度，有丝分裂原结合减少或抑制作用。AC活性不依赖于AC上Ia抗原的存在。研究结果讨论了丝裂原诱导T细胞活化的机制。
In a model system for accessory cell (AC)-dependent mitogen-induced T cell proliferation the response of several human antigen-specific, HLA-restricted helper T lymphocyte clones (HTLC) to mitogens [concanavalin A, phytohemagglutinin, staphylococcal protein A, pokeweed mitogen] was studied. The HTLC themselves did not or only weakly respond to various mitogens or to oxidation by galactose oxidase, but the response could be strongly increased if certain tumor cell lines were added to the assay as AC. Pretreatment with lectins or oxidation of either HTLC or AC was effective in stimulating the proliferation of the T cells in this system. Reduction of the aldehydes formed during oxidation completely abolished the stimulatory activity of oxidized B lymphoblastoid cell line. This shows that crosslinking of T cell and AC is required to induce proliferation. When several established cell lines were tested for their capacity to function as AC in this system, profound differences in AC activity were detected. The inability of cells with poor AC activity to stimulate the HTLC was not due to trivial reasons, such as requirements for different mitogen concentrations, a decreased binding of mitogens or suppressive effects. AC activity was not dependent on the presence of Ia antigens on the AC. The findings are discussed with regard to the mechanism of mitogen-induced T cell activation.