Kameoka J, Sato T, Torimoto Y, Sugita K, Soiffer R J, Schlossman S F, Ritz J, Morimoto C
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.
Blood. 1995 Feb 15;85(4):1132-7.
Patients who have undergone allogeneic bone marrow transplantation (allo-BMT) are susceptible to a variety of opportunistic infectious complications in the months to years after engraftment. Impaired in vitro T-cell functions have been documented in these patients, and these T-cell dysfunctions contribute to the prolonged immune deficiency after allo-BMT. In the present study, we examined the expression of CD26 as well as the reconstitution of CD26-mediated T-cell costimulation via the CD3 and CD2 pathways at various times in patients aged greater than 18 years after CD6-positive, T-cell depleted allo-BMT. We found that the percentage of CD26- and CD3-positive cells, as well as the levels of expression of both antigens, was lower than in normal controls during the first 4 months after CD6-depleted allo-BMT. Subsequently, the amount of lymphocytes expressing CD3 and CD26 and the quantitative surface expression of CD3 and CD26 were not significantly different in patients and normal controls. Functional studies showed that CD26-mediated T-cell proliferation via the CD3 pathway was considerably improved and almost reached normal levels by 1 year, whereas recovery of CD26-mediated T-cell proliferation via the CD2 pathway was delayed for at least 2 years after CD6-depleted allo-BMT. As CD26 involvement in the regulation of human thymocyte activation is restricted preferentially to the CD3 pathway--unlike its involvement with both CD3 and CD2 pathways of peripheral T cells--our results suggest that the different effects of CD26-mediated costimulation via the CD3 and CD2 pathways after CD6-depleted allo-BMT may be a reflection of peripheral T-cell immaturity in those individuals, similar to that seen in mature medullary thymocytes or cord T lymphocytes.
接受异基因骨髓移植（allo - BMT）的患者在植入后的数月至数年易发生多种机会性感染并发症。这些患者体内已被证明存在体外T细胞功能受损的情况，且这些T细胞功能障碍导致allo - BMT后免疫缺陷期延长。在本研究中，我们检测了年龄大于18岁的患者在接受CD6阳性、T细胞去除的allo - BMT后的不同时间点CD26的表达情况，以及通过CD3和CD2途径的CD26介导的T细胞共刺激的重建情况。我们发现，在CD6去除的allo - BMT后的前4个月，CD26和CD3双阳性细胞的百分比以及两种抗原的表达水平均低于正常对照。随后，患者和正常对照中表达CD3和CD26的淋巴细胞数量以及CD3和CD26的定量表面表达无显著差异。功能研究表明，到1年时，通过CD3途径的CD26介导的T细胞增殖得到显著改善，几乎达到正常水平，而在CD6去除的allo - BMT后，通过CD2途径的CD26介导的T细胞增殖恢复至少延迟2年。由于CD26对人胸腺细胞激活的调节作用优先局限于CD3途径，这与它对外周T细胞的CD3和CD2途径均有作用不同，我们的结果表明，CD6去除的allo - BMT后通过CD3和CD2途径的CD26介导的共刺激的不同效应可能反映了这些个体外周T细胞的不成熟，类似于成熟髓质胸腺细胞或脐带T淋巴细胞的情况。
