Wenzel Joerg, Tüting Thomas
Department of Dermatology, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany.
Exp Dermatol. 2007 May;16(5):454-63. doi: 10.1111/j.1600-0625.2007.00556.x.
Cutaneous lupus erythematosus (CLE) is one of the most common dermatological autoimmune disorders worldwide. Recently, several studies provided evidence for a pathogenic role of type I interferons (IFNs) in this disease. Plasmacytoid dendritic cells are major type I IFN producers in CLE skin lesions. Type I IFNs are able to induce the expression of several proinflammatory chemokines, including CXCL9 and 10, and enhance the cytotoxic capacity of infiltrating cells. Additionally, adhesion molecules and chemokine receptors, such as intercellular adhesion molecule-1, cutaneous lymphocyte antigen, E-selectin, CCR4 and CXCR3, are involved in the recruitment of potentially autoreactive lymphocytes into the skin. Here, we review the role of type I IFNs, adhesion molecules and chemokine receptors in CLE and discuss options for novel therapeutic approaches.
皮肤红斑狼疮（CLE）是全球最常见的皮肤科自身免疫性疾病之一。最近，多项研究证明I型干扰素（IFN）在该疾病中具有致病作用。浆细胞样树突状细胞是CLE皮肤病变中I型干扰素的主要产生细胞。I型干扰素能够诱导包括CXCL9和10在内的多种促炎趋化因子的表达，并增强浸润细胞的细胞毒性能力。此外，黏附分子和趋化因子受体，如细胞间黏附分子-1、皮肤淋巴细胞抗原、E-选择素、CCR4和CXCR3，参与了潜在自身反应性淋巴细胞向皮肤的募集。在此，我们综述了I型干扰素、黏附分子和趋化因子受体在CLE中的作用，并讨论了新型治疗方法的选择。
