Human cytolytic T lymphocyte interactions with vascular endothelium and fibroblasts: role of effector and target cell molecules.
Human cytolytic T lymphocyte interactions with vascular endothelium and fibroblasts: role of effector and target cell molecules.
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DOI：
10.4049/jimmunol.133.4.1878
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发表时间：
1984-10
影响因子：
4.4
通讯作者：
T. Collins;A. Krensky;C. Clayberger;W. Fiers;M. Gimbrone;S. Burakoff;J. Pober
中科院分区：
文献类型：
--
作者：
T. Collins;A. Krensky;C. Clayberger;W. Fiers;M. Gimbrone;S. Burakoff;J. Pober
针对细胞表面结构的单克隆抗体（mAb）已用于鉴定参与人溶细胞T淋巴细胞（CTL）与淋巴和其他骨髓来源靶点相互作用的几种分子。然而，在同种异体移植物排斥或移植物抗宿主病中，主要的细胞靶是血管和基质细胞，尤其是内皮细胞。然而，对于CTL与这些细胞类型的相互作用是否涉及相同的细胞表面分子知之甚少。我们评估了抗效应细胞或靶细胞结构的mAb通过克隆的人CTL系抑制易感的培养的人血管内皮细胞或真皮成纤维细胞的细胞溶解的能力。使用与T3、T4、LFA-1、LFA-2、LFA-3和HLA-DR反应的mAb，我们发现了与先前通过使用相同的CTL克隆针对淋巴靶建立的细胞溶解抑制定性相似但定量不同的模式。这些结果具有两个含义：1）CTL分子如T4、LFA-1和LFA-2识别的靶细胞结构存在于不同的细胞类型上;以及2）这种相互作用的相对重要性可能随靶细胞类型而变化。此外，我们的研究为相互作用分子的机制提供了一些见解。我们的模型系统，并使用病理生理学上重要的靶细胞，可能是有用的进一步分析CTL介导的免疫损伤。
Monoclonal antibodies (mAb) against cell surface structures have been used to identify several molecules involved in the interaction of human cytolytic T lymphocytes (CTL) with lymphoid and other bone marrow-derived targets. In allograft rejection or in graft-vs-host disease, however, major cellular targets are vascular and stromal cells, especially endothelium. Yet little is known about whether the same cell surface molecules are involved in the interactions of CTL with these cell types. We assessed the ability of mAb against effector or target cell structures to inhibit cytolysis of susceptible, cultured human vascular endothelium or dermal fibroblasts by a cloned human CTL line. Using mAb reactive with T3, T4, LFA-1, LFA-2, LFA-3, and HLA-DR, we found a qualitatively similar but quantitatively different pattern of inhibition of cytolysis as previously established for lymphoid targets by using the same CTL clone. These results have two implications: 1) the target cell structures recognized by CTL molecules such as T4, LFA-1 and LFA-2 are present on diverse cell types; and 2) the relative importance of such interactions may vary with target cell type. Furthermore, our studies provide several insights into the mechanisms of the interacting molecules. Our model system, and the use of pathophysiologically important target cells, may be useful for further analysis of CTL-mediated immune injury.