Vetter D, Gut J P, Doffoël M, Reville M, Bockel R, Kirn A
Service d'Hépatogastroentérologie, Clinique Médicale B, Hôpital Central.
Gastroenterol Clin Biol. 1989 Jan;13(1):60-5.
The T lymphocyte suppressor cell activity has been evaluated in 33 alcoholic patients compared with 16 normal controls, using an in vitro test. Suppressor T cells were activated with concanavalin A, and suppressor effect was quantified by the inhibition of an autologous B cell culture response to Pokeweed Mitogen. When compared with controls, cirrhotic patients showed a significant defect of suppressor cell activity on B cell production of IgG (20 +/- 3 vs 46 +/- 5 p. 100, p less than 0.001) and IgM (26 +/- 4 vs 56 +/- 8 p. 100, p less than 0.05). In cirrhotic patients, defect of T cell suppressor function was independent of sex and severity of the cirrhosis (Child's staging). This defect was more marked in cirrhotics with serological markers of hepatitis B virus (HBV) infection (n = 11) than in cirrhotics without markers (n = 22) (9 +/- 5 vs 25 +/- 3 p. 100, p less than 0.05; 16 +/- 6 vs 30 +/- 5 p. 100, p less than 0.05 respectively for IgG and IgM production suppression). These results suggest that HBV and lymphocytes interact directly. This interaction could increase the T suppressor cell defect, and explain the promoting role of HBV infection in the constitution of the cirrhosis in alcoholics even when viral replication is not serologically apparent.
采用体外试验，对33例酒精性患者与16例正常对照者的T淋巴细胞抑制细胞活性进行了评估。用刀豆球蛋白A激活抑制性T细胞，通过抑制自体B细胞对商陆有丝分裂原的培养反应来定量抑制作用。与对照组相比，肝硬化患者在B细胞产生IgG（20±3对46±5/100，p<0.001）和IgM（26±4对56±8/100，p<0.05）方面显示出抑制细胞活性的显著缺陷。在肝硬化患者中，T细胞抑制功能缺陷与性别和肝硬化严重程度（Child分期）无关。在有乙型肝炎病毒（HBV）感染血清学标志物的肝硬化患者（n = 11）中，这种缺陷比无标志物的肝硬化患者（n = 22）更明显（IgG和IgM产生抑制分别为9±5对25±3/100，p<0.05；16±6对30±5/100，p<0.05）。这些结果表明HBV与淋巴细胞直接相互作用。这种相互作用可能会增加T抑制细胞缺陷，并解释即使在血清学上病毒复制不明显时，HBV感染在酒精性肝硬化形成中的促进作用。
