Cole D, Van Epps D E, Williams R C
Clin Immunol Immunopathol. 1986 Feb;38(2):209-21. doi: 10.1016/0090-1229(86)90139-x.
Lymphocytes from 22 patients with established malignancy were stimulated with concanavalin A (Con A), and supernatants were tested for T-lymphocyte chemotactic factor (LCF). LCF activity was measured using a leading front chemotaxis assay with normal human T cells as responders. Fifteen of the 22 patients tested produced LCF at a level of less than 2 standard deviation below the mean of control cells. In 10 patients where mononuclear cells were stimulated with Con A for 24, 48, and 72 hr, LCF activity was significantly reduced at all three time points averaging 38, 14, and 43% of control levels, respectively. In 13 of the 31 patients, patient T-cell migration in response to casein was measured and compared to the production of LCF by mononuclear cells from these same patients. A significant correlation was observed indicating that both the response of T cells to a migration stimulus, and the production of T-cell-derived LCF was comparably suppressed. The reduction in LCF production by mononuclear cells from patients with established malignancy was not reversed by the addition of indomethacin to the culture system during Con A stimulation indicating that inhibition was not mediated by excessive prostaglandin production. The addition of patient mononuclear cells or T cells to normal mononuclear cells resulted in the inhibition of normal cell LCF by patient mononuclear cells or T cells. This could not be attributed to the production of a lymphocyte chemotactic inhibitor by patient cells, but appeared instead to be due to the direct inhibition of normal cell LCF synthesis or release by patient mononuclear cells or T cells. Separation of patient T cells into Leu 2 suppressor/cytotoxic or Leu 3 helper/inducer T cells showed that the inhibitory activity was associated with the Leu-2 T-cell subset. Heterologous normal Leu 2 T cells did not suppress normal mononuclear cell LCF production suggesting that patient Leu 2 T cells were functionally activated as compared to normal Leu 2 cells. The decreased production of LCF coupled with a depressed T-cell migratory activity in patients with established malignancy may in part be responsible for suppressed cellular immune reactions in these patients and possibly the impairment of tumor rejection.
用刀豆蛋白A（Con A）刺激22例确诊为恶性肿瘤患者的淋巴细胞，检测其培养上清液中的T淋巴细胞趋化因子（LCF）。采用前沿趋化分析方法，以正常人T细胞作为反应细胞来测定LCF活性。22例受检患者中有15例产生的LCF水平低于对照细胞平均值2个标准差。在10例患者中，用Con A刺激单个核细胞24、48和72小时，在所有这三个时间点LCF活性均显著降低，平均分别为对照水平的38%、14%和43%。在31例患者中的13例，检测了患者T细胞对酪蛋白的迁移反应，并与这些患者单个核细胞产生LCF的情况进行比较。观察到显著相关性，表明T细胞对迁移刺激的反应以及T细胞衍生的LCF的产生均受到同等程度的抑制。在Con A刺激期间，向培养系统中添加消炎痛并不能逆转确诊为恶性肿瘤患者单个核细胞LCF产生的减少，这表明抑制作用不是由前列腺素产生过多介导的。将患者单个核细胞或T细胞加入正常单个核细胞中，患者单个核细胞或T细胞会抑制正常细胞的LCF。这不能归因于患者细胞产生淋巴细胞趋化抑制剂，而似乎是由于患者单个核细胞或T细胞直接抑制了正常细胞LCF的合成或释放。将患者T细胞分离为Leu 2抑制/细胞毒性T细胞或Leu 3辅助/诱导T细胞，结果显示抑制活性与Leu - 2 T细胞亚群有关。异源性正常Leu 2 T细胞不会抑制正常单个核细胞的LCF产生，这表明与正常Leu 2细胞相比，患者Leu 2 T细胞在功能上被激活。确诊为恶性肿瘤患者中LCF产生减少以及T细胞迁移活性降低，可能部分导致了这些患者细胞免疫反应受到抑制，并可能导致肿瘤排斥受损。
