Djemadji-Oudjiel N, Goerdt S, Kodelja V, Schmuth M, Orfanos C E
Hôpital Central de N'Djamena, Tschad.
Arch Dermatol Res. 1996 Nov;288(12):757-64. doi: 10.1007/BF02505293.
Immunological mechanisms play an important role in the pathogenesis of psoriasis. Lesional psoriatic skin-derived T-cell clones have been shown to stimulate keratinocyte proliferation and to predominantly express a T-helper type 1 cytokine pattern. However, T-helper type 2-like cytokines have also been identified in some psoriatic T-cell clones. In parallel to the T-helper type 1/type 2 dichotomy, a distinction between interferon-gamma-induced (classically activated) macrophages and interleukin-4/glucocorticoid-induced (alternatively activated) macrophages has been put forward as a conceptual framework for a better understanding of immunopathological processes. In the present study, the phenotype of mononuclear phagocytes in psoriatic skin lesions (n = 21), allergic contact dermatitis (n = 4) and normal skin (n = 2) was investigated using a panel of monoclonal antibodies (mAb) against monocytes/macrophages and dendritic cells (mAb MS-1, RM 3/1, and 25F9 against subsets of in vitro alternatively activated macrophages, and mAb against myeloid antigens CD1a, CD11b, CD11c, CD34, CD36, and CD68). With regard to mononuclear phagocytes, psoriatic skin was found to be compartmentalized into epidermis, subepidermal space, and upper and lower dermis. RM 3/1++ +, MS-1+/-, 25F9- dendritic macrophages previously classified as type II alternatively activated macrophages were the dominant dermal macrophage population in psoriatic skin, while intraepidermal and epithelium-lining macrophages expressed a different, presumably classically activated, macrophage phenotype (RM 3/1-, MS-1-, 25F9-, CD68+2, CD11b+2). In allergic contact dermatitis, a classical T-helper type 1 disease, RM 3/1++ + macrophages were less prominent. Since MS-1 high molecular weight protein is much more sensitive to interferon-gamma-induced suppression than RM 3/1 antigen, a predominance of T-helper type 1 cytokines in psoriasis could explain why dermal dendritic macrophages do not express the fully induced MS-1++ +, RM 3/1++ +, 25F9+/- phenotype of type I alternatively activated macrophages.
免疫机制在银屑病的发病机制中起重要作用。已显示病变的银屑病皮肤来源的T细胞克隆可刺激角质形成细胞增殖,并主要表达1型辅助性T细胞细胞因子模式。然而,在一些银屑病T细胞克隆中也发现了类似2型辅助性T细胞的细胞因子。与1型辅助性T细胞/2型辅助性T细胞二分法并行,有人提出将干扰素-γ诱导(经典活化)的巨噬细胞和白细胞介素-4/糖皮质激素诱导(替代活化)的巨噬细胞区分开来,作为更好理解免疫病理过程的概念框架。在本研究中,使用一组针对单核细胞/巨噬细胞和树突状细胞的单克隆抗体(mAb)(针对体外替代活化巨噬细胞亚群的mAb MS-1、RM 3/1和25F9,以及针对髓系抗原CD1a、CD11b、CD11c、CD34、CD36和CD68的mAb),研究了银屑病皮肤病变(n = 21)、过敏性接触性皮炎(n = 4)和正常皮肤(n = 2)中单核吞噬细胞的表型。关于单核吞噬细胞,发现银屑病皮肤分为表皮、表皮下间隙以及真皮上层和下层。先前分类为II型替代活化巨噬细胞的RM 3/1 +++、MS-1+/-、25F9-树突状巨噬细胞是银屑病皮肤中主要的真皮巨噬细胞群体,而表皮内和上皮内衬巨噬细胞表达不同的、可能是经典活化的巨噬细胞表型(RM 3/1-、MS-1-、25F9-、CD68+2、CD11b+2)。在过敏性接触性皮炎(一种典型的1型辅助性T细胞疾病)中,RM 3/1 +++巨噬细胞不那么突出。由于MS-1高分子量蛋白比RM 3/1抗原对干扰素-γ诱导的抑制更敏感,银屑病中1型辅助性T细胞细胞因子占优势可以解释为什么真皮树突状巨噬细胞不表达I型替代活化巨噬细胞完全诱导的MS-1 +++、RM 3/1 +++、25F9+/-表型。