Takeuchi T, Rudd C E, Tanaka S, Rothstein D M, Schlossman S F, Morimoto C
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.
Eur J Immunol. 1989 Apr;19(4):747-55. doi: 10.1002/eji.1830190427.
In the present study, we have investigated the molecular basis for the immunoregulatory function of CD8 cells after autologous mixed lymphocyte reaction (AMLR) activation. We demonstrated that the CD8+CD45R+, but not the CD8+CD45R- subset of cells effected suppression following AMLR activation. In contrast, cytotoxic activity against alloantigens resided in both the CD8+CD45R+ and CD8+CD45R- subsets of cells. Biochemical analysis showed that on CD8 cells, the 220-kDa isoform of the LCA/T200 antigen family was better represented than the 200-kDa isoform, when compared to CD4 cells. The density of the CD45R antigen increased on CD8 cells following activation in AMLR and treatment of AMLR-activated CD8 cells with either anti-CD45R antibody or anti-CD3 antibody abolished the suppressor function of these cells. In contrast, treatment of AMLR-activated CD4 cells with anti-CD45R, but not anti-CD3 antibody, abolished the suppressor/inducer function of these cells. The results suggest that the CD45R antigen as well as CD3 T cell receptor complex have an important role in the suppressor function of AMLR-activated CD8 cells.
在本研究中,我们探究了自体混合淋巴细胞反应(AMLR)激活后CD8细胞免疫调节功能的分子基础。我们证明,AMLR激活后发挥抑制作用的是CD8+CD45R+细胞亚群,而非CD8+CD45R-细胞亚群。相反,针对同种异体抗原的细胞毒性活性存在于CD8+CD45R+和CD8+CD45R-细胞亚群中。生化分析表明,与CD4细胞相比,CD8细胞上LCA/T200抗原家族的220-kDa异构体比200-kDa异构体表达得更好。在AMLR中激活后,CD8细胞上CD45R抗原的密度增加,用抗CD45R抗体或抗CD3抗体处理AMLR激活的CD8细胞可消除这些细胞的抑制功能。相反,用抗CD45R而非抗CD3抗体处理AMLR激活的CD4细胞可消除这些细胞的抑制/诱导功能。结果表明,CD45R抗原以及CD3 T细胞受体复合物在AMLR激活的CD8细胞的抑制功能中起重要作用。