Estrada-G Iris, Garibay-Escobar Adriana, Núñez-Vázquez Angela, Hojyo-Tomoka Teresa, Vega-Memije Elisa, Cortés-Franco Roberto, Pérez-Uribe Adriana, Flores-Romo Leopoldo, Santos-Argumedo Leopoldo, Estrada-Parra Sergio, Domínguez-Soto Luciano
Depto. de Inmunología, Escuela Nacional de Ciencias Biológicas, IPN, Centro de Investigaciones y Estudios Avanzados, IPN, México, DF.
Int J Dermatol. 2004 Dec;43(12):893-7. doi: 10.1111/j.1365-4632.2004.02274.x.
Actinic prurigo (AP) is a photodermatosis with a restricted ethnic distribution, mainly affecting Mestizo women (mixed Indian and European). The lesions are polymorphic and include macules, papules, crusts, hyperpigmentation and lichenification. Thalidomide, an effective immunomodulatory drug, was first used successfully to treat AP in 1973. In this work we describe the effect that thalidomide had on TNF-alpha sera levels and on IL-4- and IFN gamma (IFNgamma)-producing lymphocytes of actinic prurigo (AP) patients.
Actinic prurigo patients were analyzed before and after thalidomide treatment. The percentage of IL-4+ or IFNgamma+ CD3+ lymphocytes was analyzed in eight of them by flow cytometry. TNFalpha in sera was measured by ELISA in 11 patients.
A direct correlation was observed between resolution of AP lesions and an increase in IFNgamma+ CD3+ peripheral blood mononuclear cells (P < or = 0.001) and a decrease in TNFalpha serum levels (no statistical difference). No IL-4+ CD3+ cells were detected.
Our findings confirm that AP is a disease that has an immunological component and that thalidomide clinical efficacy is exerted not only through inhibition of TNFalpha synthesis, but also through modulation of INFgamma-producing CD3+ cells. These cells could be used as clinical markers for recovery.
光化性痒疹（AP）是一种种族分布受限的光皮肤病，主要影响梅斯蒂索女性（印第安人和欧洲人的混血）。其损害具有多形性，包括斑疹、丘疹、结痂、色素沉着和苔藓化。沙利度胺是一种有效的免疫调节药物，1973年首次成功用于治疗AP。在本研究中，我们描述了沙利度胺对光化性痒疹（AP）患者血清肿瘤坏死因子-α（TNF-α）水平以及产生白细胞介素-4（IL-4）和干扰素-γ（IFNγ）的淋巴细胞的影响。
对光化性痒疹患者在沙利度胺治疗前后进行分析。其中8例患者通过流式细胞术分析IL-4+或IFNγ+ CD3+淋巴细胞的百分比。11例患者通过酶联免疫吸附测定法（ELISA）检测血清中的TNF-α。
观察到AP损害的消退与IFNγ+ CD3+外周血单个核细胞增加（P≤0.001）以及TNF-α血清水平降低（无统计学差异）之间存在直接相关性。未检测到IL-4+ CD3+细胞。
我们的研究结果证实，AP是一种具有免疫成分疾病，沙利度胺的临床疗效不仅通过抑制TNF-α合成发挥作用，还通过调节产生INFγ的CD3+细胞发挥作用。这些细胞可作为恢复的临床标志物。
