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CD8在细胞毒性T淋巴细胞介导的葡萄球菌肠毒素B裂解中的作用。

Role of CD8 in staphylococcal enterotoxin B-mediated lysis by cytotoxic T lymphocytes.

作者信息

Hoo W S, Kranz D M

机构信息

Department of Biochemistry, University of Illinois, Urbana 61801.

出版信息

J Immunol. 1993 May 15;150(10):4331-7.

PMID:8482838
Abstract

Recent evidence has suggested that recognition of superantigens such as the staphylococcal enterotoxins by CTL occurs independently of the accessory molecule CD8. These conclusions are based on the observation that antibodies to CD8 do not appear to be effective inhibitors of T cell lysis that is mediated by enterotoxin. This is in contrast to the well-known inhibitory effects of anti-CD8 antibodies on T cell activation by most peptide/class I complexes. In this study, we show that lysis of staphylococcus enterotoxin B (SEB)-bearing target cells by the mouse alloreactive CTL clone 2C is inhibited by anti-CD8 antibodies. SEB-mediated lysis by a polyclonal population of mouse CTL was also inhibited by anti-CD8 antibodies, but only under conditions where the SEB concentration is low. Inhibition occurs even when class I negative Daudi cells are used as targets. Thus, the observed inhibition does not appear to be due to the prevention of intercellular interactions between CD8 and class I molecules but is probably a consequence of preventing the intracellular association of CD8 and TCR. At the high ligand densities used in most previous studies, very few of the CD8/TCR complexes may be required for activation. Under these conditions, lysis may appear to be CD8 "independent" because 1) there are a sufficient number of preexisting CD8/TCR complexes for activation; or 2) prohibitively high concentrations of antibody would be needed to saturate unassociated CD8.

摘要

最近有证据表明,细胞毒性T淋巴细胞(CTL)对诸如葡萄球菌肠毒素等超抗原的识别独立于辅助分子CD8。这些结论基于以下观察结果:抗CD8抗体似乎不是肠毒素介导的T细胞裂解的有效抑制剂。这与抗CD8抗体对大多数肽/MHC I类复合物介导的T细胞活化的众所周知的抑制作用形成对比。在本研究中,我们表明,小鼠同种异体反应性CTL克隆2C对携带葡萄球菌肠毒素B(SEB)的靶细胞的裂解受到抗CD8抗体的抑制。抗CD8抗体也抑制了小鼠CTL多克隆群体介导的SEB裂解,但仅在SEB浓度较低的条件下。即使使用I类阴性的Daudi细胞作为靶细胞,也会出现抑制作用。因此,观察到的抑制作用似乎不是由于阻止了CD8与MHC I类分子之间的细胞间相互作用,而是可能是阻止了CD8与T细胞受体(TCR)的细胞内缔合的结果。在大多数先前研究中使用的高配体密度下,激活可能只需要极少数的CD8/TCR复合物。在这些条件下,裂解可能看起来是CD8“非依赖性”的,因为1)有足够数量的预先存在的CD8/TCR复合物用于激活;或者2)需要高得令人望而却步的抗体浓度才能饱和未结合的CD8。

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