Clinic and pathophysiology of photosensitivity in lupus erythematosus
Clinic and pathophysiology of photosensitivity in lupus erythematosus
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DOI：
10.1016/j.autrev.2008.12.012
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发表时间：
2009-05-01
影响因子：
13.6
通讯作者：
Homey, Bernhard
中科院分区：
文献类型：
--
作者：
Lehmann, Percy;Homey, Bernhard
红斑狼疮 (LE) 是一种临床变异性很大的自身免疫性疾病，其中光敏性是所有类型和亚型的共同特征。 LE 临床光敏性的性质和特征已通过标准化光测试程序阐明。紫外线损伤后皮肤损伤的发展通常会延迟，从照射后几天到三周不等，并且可能持续数月。因此，患者可能没有意识到阳光对其疾病的有害影响。 LE 对光最敏感的子集是 LE tumidus，其次是亚急性皮肤 LE。光测试对于研究 LE 光敏性的病理生理学也至关重要。 LE 中紫外线触发的凋亡细胞的产生和清除异常是自身抗原的重要来源。最近的数据证明了紫外线诱导的自身免疫反应中先天免疫途径与过继性免疫途径的联系。浆细胞样树突状细胞 (PDC) 及其分泌的 IFN-α 在 LE 发病机制中发挥着核心作用。相关白细胞亚群的募集依赖于某些趋化因子，这些趋化因子在最近的研究中得到了表征。已经假设了一个扩增循环，其中紫外线诱导细胞凋亡和坏死，从而导致趋化因子的产生和释放。随后，效应记忆 T 细胞和 PDC 被募集并激活，持续放大过程，导致紫外线诱导的皮肤 LE 病变。 (C) 2009 Elsevier B.V. 保留所有权利。
Lupus erythematosus (LE) represents an autoimmune disease with great clinical variability in which photosensitivity is a common feature for all forms and subsets. The nature and characteristics of clinical photosensitivity in LE have been elucidated through standardized phototesting procedures. The development of skin lesions after UV-injury is typically delayed starting from a few days up to three weeks after the irradiation, and may persist for months. Therefore, patients may not be aware of the detrimental effects of sunlight for their disease. The most photosensitive subset of LE is LE tumidus, followed by subacute cutaneous LE.Phototesting has also been crucial for studying the pathophysiology of LE-photosensitivity. Abnormalities of generation and clearance of UV-triggered apoptotic cells in LE are an important source of autoantigens. Recent data demonstrate the linkage of innate with adoptive immune pathways in UV-induced autoimmune response. Plasmocytoid dendritic cells (PDC) and their secreted IFN-alpha play a central role in the LE-pathogenesis. The recruitment of relevant leukocyte subsets is dependant on certain chemokines, which have been characterized in recent studies. An amplification cycle has been postulated, in which UV induces apoptosis and necrosis resulting in the production and release of chemokines. Subsequently, effector memory T cells as well as PDCs are recruited and activated perpetuating an amplification process that leads to UV-induced cutaneous LE lesion. (C) 2009 Elsevier B.V. All rights reserved.