Previously we have shown that in autoimmune hepatitis CD4 positive lymphocytes form an immunologic synapse with hepatocytes, leading to gradual diminishing and elimination of the hepatocyte. We wondered whether a similar mechanism may occur in alcoholic hepatitis (AH) and non-alcoholic steatohepatitis (NASH). We conducted immunofluorescence studies of expression of MHCII, the binding partner of CD4, on patient liver biopsies of AH, NASH, and normal controls. In cases of alcoholic hepatitis, there was prominent sinusoidal expression of MHC II; In NASH biopsies there was comparatively lower expression of MHC II, but still more than control tissue. Immunohistochemical stain for CD4 showed CD4 positive lymphocytes closely associated with hepatocytes in AH biopsies. Furthermore, expression levels of the multifunctional cytokine IL-1α was higher in AH compared to NASH and control biopsies. These results underlie the more severe nature of alcoholic hepatitis and underscore the autoimmune mechanisms involved in the liver damage found in alcoholic hepatitis.

中文翻译：

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与非酒精性脂肪性肝炎（NASH）和正常对照组相比，酒精性肝炎（AH）中肝细胞的MHCII过表达。

先前我们已经证明，在自身免疫性肝炎中，CD4阳性淋巴细胞与肝细胞形成免疫突触，从而导致肝细胞逐渐减少和消除。我们想知道酒精性肝炎（AH）和非酒精性脂肪性肝炎（NASH）是否可能发生类似的机制。我们对AH，NASH和正常对照的患者肝活检进行了CD4结合伴侣MHCII表达的免疫荧光研究。在酒精性肝炎的病例中，MHC II有明显的正弦表达。在NASH活检中，MHC II的表达相对较低，但仍比对照组织高。CD4的免疫组织化学染色显示，AH活检中CD4阳性淋巴细胞与肝细胞紧密相关。此外，与NASH和对照活检相比，AH中多功能细胞因子IL-1α的表达水平更高。这些结果奠定了酒精性肝炎更为严重的性质，并强调了与酒精性肝炎中发现的肝损害有关的自身免疫机制。