Cuevas-Santos J, Contreras F, McNutt N S
Department of Pathology, University Hospital, Guadalajara, Spain.
J Cutan Pathol. 1998 Nov;25(10):530-7. doi: 10.1111/j.1600-0560.1998.tb01736.x.
In the defense against Mycobacterium leprae, macrophages play an essential part in the mechanism of bacterial lysis but require the presence of cytokines such as interleukin 2 and gamma interferon from lymphocytes in order to effectively kill the organisms in any number. While there have been many studies of the lymphocytes in lesions of leprosy, less attention has been given to the immunohistochemical characterization of the macrophage populations. In this study, the cutaneous lesions of 69 patients with leprosy (42 lepromatous, 5 mid-borderline, and 22 tuberculoid) were evaluated by immunohistochemistry for the expression of S100 protein, CD1a, CD68, muramidase, HLA-DR, and Factor 13a. The macrophages from lesions of polar, subpolar, and borderline lepromatous leprosy patients expressed S100 protein intensely and constantly. In contrast, the lesions of polar and subpolar tuberculoid leprosy had very few cells that were immunoreactive for S100 protein ('S100+') in the granulomas in the dermis. The macrophages in all lesions were reactive for CD68 and muramidase. In paraffin sections, macrophages of lepromatous lesions failed to stain for HLA-DR, whereas in tuberculoid lesions, they were strongly positive for HLA-DR. Three patients with histoid leprosy (relapse lesions) had lesions that were strongly positive for Factor 13a and were negative for S100 protein ('S100-'). Given the possible chemotactic and migration inhibition effects of the calcium-binding proteins of the S100 family, these data suggest a possibly important role for S100 protein in the accumulation of macrophages in lepromatous leprosy, and also reveal infection of Factor 13a + dermal dendritic cells in histoid leprosy.
在抵抗麻风分枝杆菌的过程中，巨噬细胞在细菌裂解机制中发挥着重要作用，但需要淋巴细胞产生的细胞因子（如白细胞介素2和γ干扰素）的存在，才能有效杀灭一定数量的病原体。虽然对麻风病损中的淋巴细胞已有许多研究，但对巨噬细胞群体的免疫组织化学特征关注较少。在本研究中，通过免疫组织化学方法评估了69例麻风病患者（42例瘤型、5例中间界线类和22例结核样型）皮肤损害中S100蛋白、CD1a、CD68、溶菌酶、HLA-DR和因子13a的表达。极型、亚极型和界线类偏瘤型麻风病患者病损中的巨噬细胞强烈且持续表达S100蛋白。相比之下，极型和亚极型结核样型麻风病损中，真皮肉芽肿内对S100蛋白呈免疫反应性的细胞（“S100+”）极少。所有病损中的巨噬细胞对CD68和溶菌酶均呈反应性。在石蜡切片中，瘤型病损的巨噬细胞HLA-DR染色阴性，而结核样型病损的巨噬细胞HLA-DR染色强阳性。3例组织样麻风病（复发病损）患者的病损对因子13a呈强阳性，对S100蛋白呈阴性（“S100-”）。鉴于S100家族钙结合蛋白可能具有趋化和迁移抑制作用，这些数据表明S100蛋白在瘤型麻风病巨噬细胞聚集中可能发挥重要作用，同时也揭示了组织样麻风病中因子13a+真皮树突状细胞的感染情况。
