Sundqvist K G, Hauzenberger D, Hultenby K, Bergström S E
Department of Clinical Immunology, Huddinge Hospital, Stockholm, Sweden.
Exp Cell Res. 1993 May;206(1):100-10. doi: 10.1006/excr.1993.1125.
Lymphocytes were plated on two-dimensional (2D) and three-dimensional (3D) collagen substrata and their distribution and behavior determined using light and scanning electron microscopy. When allowed to settle on 2D collagen substrate T-lymphocytes "rapidly" attached and penetrated and thus virtually never remained attached on top of the collagen. As a consequence of this penetration the cells appeared below the collagen. In contrast to lymphocytes, fibroblasts and macrophages allowed to settle on 2D collagen did not penetrate but underwent cytoplasmic spreading on top of the collagen. Lymphocyte attachment and penetration of 2D collagen was specifically inhibited by monoclonal antibodies to beta 1-integrins, indicating that the process depends on molecular adhesion to the collagen. The penetration of 2D collagen appeared to consist of tight binding of collagen fibers to the cells, local reorganization of the collagen carpet, and redistribution of the cell-attached collagen fibers from the "lower" to the "upper" pole/surface of the lymphocyte. Lymphocyte infiltration of 3D collagen substrata was also specifically inhibited by monoclonal antibodies to beta 1-integrins. During the infiltration of 3D collagen lymphocytes exhibited collagen fibers attached to their surface and seemed to provoke perturbation of the collagen. These results show that T lymphocytes are programmed to penetrate and perturb 2D and 3D collagen substrata by a mechanism dependent on adhesive interaction. However, deattachment tends to counteract persistent binding of the cells to 2D collagen.
将淋巴细胞接种在二维(2D)和三维(3D)胶原基质上,并用光学显微镜和扫描电子显微镜确定它们的分布和行为。当T淋巴细胞在2D胶原基质上沉降时,它们“迅速”附着并穿透,因此几乎不会一直附着在胶原表面。由于这种穿透,细胞出现在胶原下方。与淋巴细胞不同,接种在2D胶原上的成纤维细胞和巨噬细胞不会穿透,而是在胶原表面进行细胞质铺展。针对β1整合素的单克隆抗体可特异性抑制淋巴细胞对2D胶原的附着和穿透,这表明该过程依赖于与胶原的分子粘附。2D胶原的穿透似乎包括胶原纤维与细胞的紧密结合、胶原毯的局部重组以及细胞附着的胶原纤维从淋巴细胞的“下”极/表面重新分布到“上”极/表面。针对β1整合素的单克隆抗体也可特异性抑制淋巴细胞对3D胶原基质的浸润。在3D胶原浸润过程中,淋巴细胞表面附着有胶原纤维,并且似乎会引起胶原的扰动。这些结果表明,T淋巴细胞通过一种依赖于粘附相互作用的机制被编程为穿透并扰动2D和3D胶原基质。然而,脱离倾向于抵消细胞与2D胶原的持续结合。