Membrane tumor necrosis factor-alpha (TNF-alpha) expressed on HTLV-I-infected T cells mediates a costimulatory signal for B cell activation - Characterization of membrane TNF-alpha
Membrane tumor necrosis factor-alpha (TNF-alpha) expressed on HTLV-I-infected T cells mediates a costimulatory signal for B cell activation - Characterization of membrane TNF-alpha
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DOI：
10.1006/clin.1996.4291
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发表时间：
1997-02-01
期刊：
影响因子：
--
通讯作者：
Niho, Y
中科院分区：
文献类型：
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作者：
Higuchi, M;Nagasawa, K;Niho, Y
活化的CD4(+) T细胞上表达的26kda膜肿瘤坏死因子- α (tnf - α)是T- b细胞相互作用中功能性膜分子的新候选分子。我们发现，正常的人T细胞在体外感染I型人T淋巴细胞病毒（HTLV-I）后，被诱导表达26kda膜tnf - α。受感染的T细胞通过该分子激活自体E细胞以接触依赖的方式产生免疫球蛋白（Ig）RI，抗tnf - α抗体（Ab）部分抑制免疫球蛋白（Ig）RI。然而，可能是由于感染T细胞上缺乏CD40配体表达，抗tnf - α Ab治疗刺激了感染T细胞中白细胞介素(IL)-2和干扰素γ (ifn - γ)的分泌。这些作用不受抗tnf受体Ab治疗的诱导。抗tnf - α Ab也诱导感染T细胞内钙浓度升高。这些结果表明，表达膜tnf - α的T细胞可以通过该分子直接刺激。因此，提示htlv -i感染T细胞上的26 kda膜tnf - α α在多克隆B细胞活化中起作用，并可能参与某些htlv -i相关疾病的发病机制。此外，我们的研究结果提示了一种新的机制，即细胞因子的产生可以通过T细胞表面的膜tnf - α来调节。(C) 1997学术出版社。
The 26-kDa membrane tumor necrosis factor-alpha (TNF-alpha) expressed on activated CD4(+) T cells is a novel candidate for the functional membrane molecule in T-B cell interactions. We found that normal human T cells, when infected with human T cell lymphotropic virus type I (HTLV-I) in vitro, were induced to express the 26-kDa membrane TNF-alpha. The infected T cells, through this molecule, activated autologous E cells to produce immunoglobulin (Ig)RI in a contact-dependent manner, which was partially inhibited by anti-TNF-alpha antibody (Ab). IgG synthesis was not stimulated, however, probably because of lack of CD40 ligand expression on the infected T cells, Anti-TNF-alpha Ab treatment stimulated the secretion of interleukin (IL)-2 and interferon gamma (IFN-gamma) in the infected T cells. These effects were not induced by anti-TNF receptor Ab treatment. Anti-TNF-alpha Ab also induced the elevation of intracellular calcium concentration in the infected T cells. These results suggest that T cells expressing membrane TNF-alpha can be directly stimulated through this molecule. Thus, it is suggested that the 26-kDa membrane TNF-alpha alpha on HTLV-I-infected T cells plays a role in polyclonal B cell activation and may be involved in the pathogenesis of some HTLV-I-associated diseases. Additionally, our results suggest a novel mechanism by which cytokine production can be modulated in these T cells through membrane TNF-alpha on their surface. (C) 1997 Academic Press.