Matsuda M, Maeda Y, Shirakawa C, Masaki H, Koyama A, Horiuchi F, Hamazaki H, Fujimoto T, Irimajiri K, Horiuchi A
Third Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.
Br J Haematol. 1993 Feb;83(2):212-7. doi: 10.1111/j.1365-2141.1993.tb08274.x.
Immunological abnormality of T lymphocytes in patients with adult T cell leukemia (ATL) is characterized by abnormal expression of the 55 kD chain of the receptor for interleukin 2 (IL-2R/p55) (Tac), and the down-regulation of CD3 expression. Using serum and culture supernatants of leukaemic cells from ATL patients (Group A) whose CD3 expression was down-regulated and those (Group B) whose CD3 was not low, the possible mechanism of CD3 down-regulation on ATL cells was discussed. When PBMC from normal individuals were cultured with sera from ATL patients for 24 h, CD3 expression revealed by mean fluorescent intensity (MFI) was down-regulated by sera from ATL patients in Group A (MFI: Pt 1 = 51.6 +/- 4.5, Pt 2 = 48.0 +/- 6.9, control = 96.5 +/- 6.6), not by sera from patients in Group B (MFI: Pt 3 = 105.5 +/- 7.9, Pt 4 = 102.5 +/- 8.3, control = 96.5 +/- 6.6). When normal PBMC were cultured with supernatants of leukaemic cells from ATL patients in Group A, this CD3 down-regulating activity was also detected (MFI: Pt 1 = 78.0 +/- 10.2, Pt 2 = 70.6 +/- 8.7, control = 94.0 +/- 6.6). By using gel-chromatography, the fractionated supernatants from ATL patients in Group A decreased CD3 expression of normal PBMC significantly (MFI: Pt = 22.9 +/- 5.8, Pt 2 = 28.8 +/- 7.4, control = 92.1 +/- 9.6). This CD3 down-regulating activity in fractionated supernatant was not inhibited by any lymphokine antibodies, anti-IL-1 alpha antibody (Ab), anti-IL-1B Ab, anti-IL-2 Ab, anti-IL-3 Ab, anti-IL-4 Ab, anti-IL-6 Ab, anti-TNF-alpha Ab and anti-IFN-gamma Ab. Any known cytokines (IL-1, IL-2, IL-3, IL-4, IL-6, TNF-alpha and IFN-gamma) could not modulate CD3 expression of normal PBMC. These findings suggested that there are novel factor(s) with CD3 down-regulating activity in the serum and culture supernatant of ATL patient and those factor(s) are involved in progression of ATL.
成人T细胞白血病（ATL）患者T淋巴细胞的免疫异常表现为白细胞介素2受体（IL-2R/p55）（Tac）的55 kD链表达异常，以及CD3表达下调。利用ATL患者（A组）白血病细胞的血清和培养上清液，这些患者的CD3表达下调，以及CD3不低的患者（B组）的血清和培养上清液，探讨了ATL细胞上CD3下调的可能机制。当将正常个体的外周血单核细胞（PBMC）与ATL患者的血清培养24小时时，A组ATL患者的血清使通过平均荧光强度（MFI）显示的CD3表达下调（MFI：患者1 = 51.6±4.5，患者2 = 48.0±6.9，对照 = 96.5±6.6），而B组患者的血清则没有这种作用（MFI：患者3 = 105.5±7.9，患者4 = 102.5±8.3，对照 = 96.5±6.6）。当正常PBMC与A组ATL患者白血病细胞的上清液培养时，也检测到了这种CD3下调活性（MFI：患者1 = 78.0±10.2，患者2 = 70.6±8.7，对照 = 94.0±6.6）。通过凝胶过滤，A组ATL患者分级分离的上清液显著降低了正常PBMC的CD3表达（MFI：患者1 = 22.9±5.8，患者2 = 28.8±7.4，对照 = 92.1±9.6）。分级分离上清液中的这种CD3下调活性不受任何淋巴因子抗体的抑制，包括抗IL-1α抗体（Ab）、抗IL-1B抗体、抗IL-2抗体、抗IL-3抗体、抗IL-4抗体、抗IL-6抗体、抗TNF-α抗体和抗IFN-γ抗体。任何已知的细胞因子（IL-1、IL-2、IL-3、IL-4、IL-6、TNF-α和IFN-γ）都不能调节正常PBMC的CD3表达。这些发现表明，ATL患者的血清和培养上清液中存在具有CD3下调活性的新型因子，并且这些因子参与了ATL的进展。
