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氯喹在光敏患者紫外线B照射皮肤中的原位定位及免疫组织学研究。

In situ localization of chloroquine and immunohistological studies in UVB-irradiated skin of photosensitive patients.

作者信息

Sjölin-Forsberg G, Berne B, Eggelte T A, Karlsson-Parra A

机构信息

Department of Dermatology, University Hospital, Uppsala, Sweden.

出版信息

Acta Derm Venereol. 1995 May;75(3):228-31. doi: 10.2340/0001555575228231.

DOI:10.2340/0001555575228231
PMID:7653184
Abstract

Chloroquine can prevent photosensitivity reactions, but its mechanism of action is poorly understood. To investigate if the drug may interfere with inflammatory or immunological mechanisms of the UV-induced erythema of photosensitive patients, we studied the localization of chloroquine in the skin and its effect on the epidermal/dermal expression of IL-1, TNF-alpha, IL-6 and ICAM-1 and the occurrence of different lymphoid cells in normal skin and UVB-induced erythema in 8 patients with photosensitive discoid and systemic lupus erythematosus and 4 patients with polymorphic light eruption (PMLE), before and during chloroquine treatment. Using a specific monoclonal antibody against chloroquine, we found a strong granular staining pattern of mainly keratinocytes in all biopsy specimens from normal and erythematous skin during chloroquine treatment. In non-irradiated skin, T lymphocytes, macrophages and HLA-DR expressing cells were sparsely distributed within the dermis in similar amounts before and during chloroquine treatment. In UVB-induced erythema an increase in the number of these cells, mainly located in the dermal perivascular area, was seen before medication. During chloroquine treatment such cellular infiltration was reduced. ICAM-1 expression was detected on the endothelium of dermal vessels but not on keratinocytes. The accumulation of chloroquine in the epidermis and the decreased cellular infiltration in erythematous skin during chloroquine treatment indicate a local anti-inflammatory effect. This effect may be due to either unspecific UV-protective properties of the drug or to some specific downregulating action by chloroquine on keratinocyte function.

摘要

氯喹可预防光敏反应,但其作用机制尚不清楚。为研究该药是否会干扰光敏患者紫外线诱导红斑的炎症或免疫机制,我们在氯喹治疗前和治疗期间,研究了氯喹在皮肤中的定位及其对8例光敏性盘状红斑狼疮和系统性红斑狼疮患者以及4例多形性日光疹(PMLE)患者正常皮肤和紫外线B诱导红斑中白细胞介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和细胞间黏附分子-1(ICAM-1)的表皮/真皮表达以及不同淋巴细胞出现情况的影响。使用针对氯喹的特异性单克隆抗体,我们发现在氯喹治疗期间,来自正常皮肤和红斑皮肤的所有活检标本中,主要是角质形成细胞呈现强烈的颗粒状染色模式。在未照射的皮肤中,氯喹治疗前和治疗期间,T淋巴细胞、巨噬细胞和表达人类白细胞抗原-DR(HLA-DR)的细胞在真皮内稀疏分布,数量相似。在紫外线B诱导的红斑中,用药前可见这些细胞数量增加,主要位于真皮血管周围区域。在氯喹治疗期间,这种细胞浸润减少。ICAM-1表达在真皮血管内皮细胞上检测到,但在角质形成细胞上未检测到。氯喹在表皮中的蓄积以及氯喹治疗期间红斑皮肤中细胞浸润的减少表明其具有局部抗炎作用。这种作用可能是由于该药非特异性的紫外线防护特性,或者是氯喹对角质形成细胞功能的某些特异性下调作用。

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