Chisari F V, Castle K L, Xavier C, Anderson D S
J Immunol. 1981 Jan;126(1):38-44.
Hepatocellular injury in hepatitis B virus infection may be produced by an autoaggressive hepatocytotoxic immune response. To test the hypothesis that acquired suppressor cell defects may participate in such a response, we assessed the functional integrity of 2 suppressor cell populations in patients with type B viral hepatitis. Spontaneous suppression of the 1-way mixed lymphocyte response by radiation-resistant, adherent peripheral blood mononuclear cells decreases during the acute phase of disease, returns towards normal with clinical recovery, but remains depressed in patients with chronic hepatitis. The degree of spontaneous suppressor cell dysfunction correlates inversely with at least 1 biochemical parameter of hepatocellular injury (SGPT). The functional integrity of this suppressor cell fluctuates during chronic hepatitis and may reflect currently undefined biologic variables in this disease. Mitogen-induced suppression on lymphocyte activation by radiation resistant, nonadherent suppressor cells is also depressed in acute and chronic hepatitis, but it does not correlate with biochemical evidence of hepatocellular injury on an individual-patient basis. Documentation of these generalized defects of nonspecific suppressor cell function establishes a basis for the possible existence of specific anomalies of immuno-regulation that may permit the expression of normally suppressed auoaggressive hepatocytotoxic immune mechanisms in viral hepatitis.
乙型肝炎病毒感染中的肝细胞损伤可能由自身攻击性肝细胞毒性免疫反应所致。为验证获得性抑制细胞缺陷可能参与这种反应这一假说，我们评估了B型病毒性肝炎患者中2种抑制细胞群的功能完整性。在疾病急性期，具有辐射抗性的贴壁外周血单核细胞对单向混合淋巴细胞反应的自发抑制作用减弱，随着临床康复恢复正常，但在慢性肝炎患者中仍处于抑制状态。自发抑制细胞功能障碍的程度与肝细胞损伤的至少1项生化指标（谷丙转氨酶）呈负相关。这种抑制细胞的功能完整性在慢性肝炎期间波动，可能反映了该疾病中目前尚未明确的生物学变量。具有辐射抗性的非贴壁抑制细胞对淋巴细胞激活的丝裂原诱导抑制作用在急性和慢性肝炎中也受到抑制，但在个体患者中它与肝细胞损伤的生化证据无相关性。这些非特异性抑制细胞功能普遍缺陷的证据为免疫调节可能存在特异性异常奠定了基础，这种异常可能使病毒性肝炎中正常被抑制的自身攻击性肝细胞毒性免疫机制得以表达。
