Serjeantson S, Dry P
Clin Exp Immunol. 1980 Feb;39(2):289-96.
Serum lymphocytotoxic antibodies (LCAs) were detected in 67% of Papua New Guinean lepromatous leprosy patients who were persistent carriers of hepatitis B surface antigen (HBsAg). Lymphocytotoxins were not associated with asymptomatic HBsAg in either healthy controls or tuberculoid leprosy patients. It was apparent that, although HBsAg itself is a poor indicator of in vitro lymphocytotoxicity, when the antigen occurred in a host with impaired immune response, lymphocytotoxicity, when the antigen occurred in a host with impaired immune response, lymphocytotoxicity was enhanced. In contrast to this finding, lepromatous leprosy patients without HBsAg had significantly depressed LCA production in comparison with tuberculoid patients and controls. The interaction between leprosy and hepatitis B virus was highly significant (P = 0.001) in an analysis of variance of cytotoxicity scores. It is proposed that the previously reported equivocal results regarding autoantibodies in leprosy patients may be explained by this unusual interaction between lepromatous leprosy and hepatitis B virus infection.
在巴布亚新几内亚持续性携带乙肝表面抗原(HBsAg)的瘤型麻风患者中,67%检测到血清淋巴细胞毒性抗体(LCAs)。在健康对照者或结核样型麻风患者中,淋巴细胞毒素与无症状HBsAg均无关联。显然,尽管HBsAg本身并非体外淋巴细胞毒性的良好指标,但当该抗原出现在免疫反应受损的宿主中时,淋巴细胞毒性会增强。与这一发现相反,未感染HBsAg的瘤型麻风患者与结核样型患者及对照相比,LCA产生显著降低。在细胞毒性评分的方差分析中,麻风与乙肝病毒之间的相互作用非常显著(P = 0.001)。有人提出,先前报道的麻风患者自身抗体结果不明确,可能是由瘤型麻风与乙肝病毒感染之间这种异常相互作用所解释。