Pelkonen J, Palacios R
Department of Microbiology, Kuopio University, Finland.
Int Immunol. 1990;2(6):555-62. doi: 10.1093/intimm/2.6.555.
In order to learn more about the small subset of CD4-CD8- TCR alpha beta/CD3+ peripheral T lymphocytes, we firstly characterized at the cellular and molecular levels the CD4-CD8- LD1 cell line isolated from the spleen of an MRL/lpr-lpr mouse. Secondly we studied its functional properties. LD1 cells are Thy1+ CD5+ CD4-CD8- LFA-1+ PgP-1+ and do not bind the T cell precursor-specific antibodies Joro 37-5 or Joro 75. They are negative for IgM, B-220, BP-1, J11d, Lyb8, Ia, F4/80, BP-2, and Mac-1 surface markers. LD1 cells have deleted the TCR delta locus, have rearrangements at the TCR gamma gene cluster (i.e. a V gamma 1-J gamma 1-C gamma 1 and a V gamma 4.3-J gamma 4-C gamma 4) and have two rearrangements of the TCR beta gene cluster (i.e. a D beta 1-J beta 1 and V-D-J beta 2). LD1 cells produce normal sized RNA transcripts from TCR alpha and beta genes and lower levels of gamma-mRNA. These cells bind CD3- and pan-TCR beta-specific antibodies as determined by FM analysis. We conclude that LD1 cells bear a TCR alpha beta/CD3 type of receptor complex. LD1 cells fail both in vivo and in vitro to differentiate into CD4+ or CD8+ cells. These cells help B lymphocytes to mature into antibody-secreting cells, secrete IL-3 and IL-6 but not IL-2, IL-4, or IL-5, and exert no detectable cytolytic activity. These results together with recent reports of antigen-specific CD4-CD8- TCR alpha beta/CD3+ cytotoxic T cell lines show that the CD4-CD8- TCR alpha beta/CD3+ subset comprises functionally competent helper and cytotoxic T lymphocytes and thereby argue for their potential to participate in immune responses. Our results also suggest that cells like LD1 represent terminally differentiated T lymphocytes rather than cells with precursor potential for CD4+ or CD8+ TCR alpha beta/CD3+ T lymphocytes.
为了更深入了解CD4-CD8-TCRαβ/CD3+外周T淋巴细胞的小亚群,我们首先在细胞和分子水平上对从MRL/lpr-lpr小鼠脾脏中分离出的CD4-CD8-LD1细胞系进行了表征。其次,我们研究了其功能特性。LD1细胞为Thy1+CD5+CD4-CD8-LFA-1+PgP-1+,不与T细胞前体特异性抗体Joro 37-5或Joro 75结合。它们的IgM、B-220、BP-1、J11d、Lyb8、Ia、F4/80、BP-2和Mac-1表面标志物均为阴性。LD1细胞已缺失TCRδ基因座,在TCRγ基因簇处发生重排(即Vγ1-Jγ1-Cγ1和Vγ4.3-Jγ4-Cγ4),并且TCRβ基因簇有两种重排(即Dβ1-Jβ1和V-D-Jβ2)。LD1细胞从TCRα和β基因产生正常大小的RNA转录本,γ-mRNA水平较低。通过流式细胞术分析确定,这些细胞可结合CD3和泛TCRβ特异性抗体。我们得出结论,LD1细胞带有TCRαβ/CD3类型的受体复合物。LD1细胞在体内和体外均无法分化为CD4+或CD8+细胞。这些细胞帮助B淋巴细胞成熟为抗体分泌细胞,分泌IL-3和IL-6,但不分泌IL-2、IL-4或IL-5,并且没有可检测到的细胞溶解活性。这些结果与最近关于抗原特异性CD4-CD8-TCRαβ/CD3+细胞毒性T细胞系的报道一起表明,CD4-CD8-TCRαβ/CD3+亚群包含功能上有活性的辅助性和细胞毒性T淋巴细胞,因此证明它们有参与免疫反应的潜力。我们的结果还表明,像LD1这样的细胞代表终末分化的T淋巴细胞,而不是具有CD4+或CD8+TCRαβ/CD3+T淋巴细胞前体潜能的细胞。