Gottlieb A B
Laboratory of Investigative Dermatology, Rockefeller University, New York, NY 10021.
J Am Acad Dermatol. 1988 Jun;18(6):1376-80. doi: 10.1016/s0190-9622(88)70145-0.
This review presents evidence for the immunopathogenesis of psoriasis. T lymphocytes with human lymphocyte antigen (HLA)-DR molecules and receptors for interleukin 2 were found in the dermis of psoriatic plaques, suggesting the presence of activated T cells in these lesions. Keratinocytes in active plaques demonstrated HLA-DR molecules on their surfaces. These immunologic abnormalities were reversible with medical therapy. Keratinocyte HLA-DR expression was associated with an increased incidence of psoriatic arthritis. We propose that HLA-DR + keratinocytes and Langerhans cells in plaques could activate dermal T cells directly in an autologous mixed leucocyte/epithelial cell reaction. Alternatively, they could present an unknown autologous or exogenous antigen to T lymphocytes. T cell activation would then lead to the release of mediators of inflammation, and possibly of epidermal growth factors. This hypothesis also provides an explanation for the chronicity of psoriasis. Most of the therapies used to treat psoriasis suppress cellular immune function and inflammation. These include ultraviolet irradiation, cyclosporine, corticosteroids, methotrexate, anthralin, and retinoids.
本综述展示了银屑病免疫发病机制的证据。在银屑病斑块的真皮层中发现了带有人类淋巴细胞抗原（HLA）-DR分子和白细胞介素2受体的T淋巴细胞，这表明这些病变中存在活化的T细胞。活跃斑块中的角质形成细胞在其表面展示出HLA-DR分子。这些免疫异常通过药物治疗是可逆的。角质形成细胞HLA-DR表达与银屑病关节炎发病率增加相关。我们提出，斑块中的HLA-DR +角质形成细胞和朗格汉斯细胞可在自体混合白细胞/上皮细胞反应中直接激活真皮T细胞。或者，它们可以将未知的自体或外源性抗原呈递给T淋巴细胞。T细胞活化随后会导致炎症介质以及可能的表皮生长因子的释放。这一假说也为银屑病的慢性病程提供了解释。用于治疗银屑病的大多数疗法会抑制细胞免疫功能和炎症。这些疗法包括紫外线照射、环孢素、皮质类固醇、甲氨蝶呤、蒽林和维甲酸。
