Swartz T J, Evavold B, Suzuki H, Yokoyama A, Quintans J
Department of Medicine, University of Chicago, Illinois 60637.
Transplantation. 1988 Jul;46(1):137-43. doi: 10.1097/00007890-198807000-00025.
T cell blasts and lines passively acquire MHC molecules in vitro. To determine the role of these molecules in immunoregulatory reactions, we examined whether T cell lines grown on irradiated F1 spleen cells were able to supply allogeneic MHC antigens for the stimulation of T cell proliferation. Immunofluorescence analysis demonstrates that autoreactive T cell lines grown with irradiated F1 spleen cells acquire allogeneic class II molecules and subsequently lose the MHC molecules within 4 days of coculture with syngeneic cells. The proliferative response of (H-2k x H-2d)F1T cells stimulated by a T cell line grown on (H-2k x H-2d)F1 cells is inhibited by the addition of hybridoma-culture supernatants containing anti-IAd as well as anti-IEk antibodies. The proliferation of the F1 T cells to the T cell line grown on H-2k spleen cells is only affected by supernatants containing anti-IEk antibodies. To investigate the role of acquired class I MHC antigens, we examined their ability to serve as antigens for cytotoxic cells. Anti-H-2k cytotoxic T cells are generated when H-2b T cells are cultured with an H-2b-derived T cell line, only if the line has been grown on (H-2k x H-2b)F1 cells. An H-2b-derived T cell line exposed to (H-2k x H-2b)F1 cells can be lysed by anti-H-2k cytotoxic T cells from a primary MLR. Similarly, an H-2k anti-H-2b cytotoxic T cell clone will kill an H-2k-derived T cell clone grown on (H-2k x H-2b)F1 spleen cells. These results demonstrate that passively acquired class I molecules can stimulate the generation of cytotoxic T cells that lyse cells expressing the class I antigens and that passively acquired class I molecules expressed on T cells serve as the target for cytotoxic T cells.
T细胞母细胞和细胞系在体外可被动获得主要组织相容性复合体（MHC）分子。为确定这些分子在免疫调节反应中的作用，我们检测了在经照射的F1脾细胞上生长的T细胞系是否能够提供同种异体MHC抗原以刺激T细胞增殖。免疫荧光分析表明，与经照射的F1脾细胞共同培养的自身反应性T细胞系获得了同种异体II类分子，随后在与同基因细胞共培养4天内失去了MHC分子。由在（H-2k×H-2d）F1细胞上生长的T细胞系刺激的（H-2k×H-2d）F1 T细胞的增殖反应，会被添加含有抗IAd以及抗IEk抗体的杂交瘤培养上清液所抑制。F1 T细胞对在H-2k脾细胞上生长的T细胞系的增殖反应仅受含有抗IEk抗体的上清液影响。为研究获得的I类MHC抗原的作用，我们检测了它们作为细胞毒性细胞抗原的能力。只有当H-2b T细胞与源自H-2b的T细胞系共同培养时，才能产生抗H-2k细胞毒性T细胞，前提是该细胞系已在（H-2k×H-2b）F1细胞上生长。暴露于（H-2k×H-2b）F1细胞的源自H-2b的T细胞系可被来自初次混合淋巴细胞反应（MLR）的抗H-2k细胞毒性T细胞裂解。同样，H-2k抗H-2b细胞毒性T细胞克隆会杀死在（H-2k×H-2b）F1脾细胞上生长的源自H-2k的T细胞克隆。这些结果表明，被动获得的I类分子可刺激细胞毒性T细胞的产生，这些细胞毒性T细胞可裂解表达I类抗原的细胞，并且T细胞上被动获得的I类分子可作为细胞毒性T细胞的靶标。
