首页> 外文期刊>Photodermatology, photoimmunology and photomedicine >Efficacy of ultraviolet A1 phototherapy on the expression of bcl-2 in atopic dermatitis and cutaneous T-cell lymphoma in vivo: a comparison study.
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Efficacy of ultraviolet A1 phototherapy on the expression of bcl-2 in atopic dermatitis and cutaneous T-cell lymphoma in vivo: a comparison study.

机译:紫外线A1光疗对体内特应性皮炎和皮肤T细胞淋巴瘤bcl-2表达的影响:一项比较研究。

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BACKGROUND/PURPOSE: Atopic dermatitis (AD) is characterized immunohistochemically by a high number of skin infiltrating T-helper cells (CD4 +). In most cases cutaneous T-cell lymphoma (CTCL) is characterized by a malignant proliferation of CD4+ T-helper lymphocytes. The purpose of our study was to evaluate the extent of anti-apoptotic effects in patients suffering from AD or CTCL, respectively, which may contribute to the prolonged inflammation. Furthermore, we investigated whether medium-dose ultraviolet A1 (UVA1) phototherapy is able to modulate the expression of bcl-2 within the dermal inflammatory infiltrate. METHODS: In order to enumerate bcl-2+ cells pre- and post-therapeutic punch skin biopsies of ten patients with AD and five patients with CTCL were stained immunohistochemically for features of apoptosis using a monoclonal antibody detecting bcl-2. RESULTS: Both AD and CTCL sections revealed a high percentage of bcl-2+ cells within the dermal perivascular infiltrate before therapy. After the successful treatment using medium-dose UVA1 phototherapy this percentage could be decreased significantly. CONCLUSION: Both T-cell-derived skin diseases exhibit an increased pre-therapeutic number of bcl-2+ cells. After medium-dose UVA1 phototherapy the substantial improvement of the skin condition was linked to a significant decrease of the dermal bcl-2+ cell count. Moreover, we could demonstrate a remarkable correlation referring to the decrease and staining pattern of bcl-2 between these two groups as well as within each group. Because the bcl-2 protein is known to act as an apoptosis inhibitor, its pre-therapeutic increase may provide the persistent cutaneous inflammatory reaction in T-cell-derived skin diseases. Additionally, the post-therapeutic reduction of bcl-2+ cells might represent a key mechanism of medium-dose UVA1 phototherapy.
机译:背景/目的:特应性皮炎(AD)的免疫组织化学特征是大量的皮肤浸润性T辅助细胞(CD4 +)。在大多数情况下,皮肤T细胞淋巴瘤(CTCL)的特征在于CD4 + T辅助淋巴细胞的恶性增殖。我们研究的目的是评估分别患有AD或CTCL的患者的抗凋亡作用的程度,这可能有助于延长炎症。此外,我们调查了中等剂量的紫外线A1(UVA1)光疗是否能够调节皮肤炎症浸润物中bcl-2的表达。方法:为了计数治疗前和治疗后穿孔穿孔皮肤活检的bcl-2 +细胞,对10例AD患者和5例CTCL患者进行免疫组织化学染色,用单克隆抗体检测bcl-2的凋亡特征。结果:AD和CTCL切片均显示治疗前皮肤血管周围浸润中bcl-2 +细胞的百分比很高。使用中等剂量的UVA1光疗成功治疗后,该百分比可以显着降低。结论:两种T细胞源性皮肤疾病的治疗前bcl-2 +细胞数量均增加。中剂量UVA1光疗后,皮肤状况的显着改善与皮肤bcl-2 +细胞计数的显着降低有关。此外,我们可以证明这两组之间以及各组内bcl-2的减少和染色模式之间存在显着的相关性。由于已知bcl-2蛋白可作为凋亡抑制剂,因此其治疗前的增加可在T细胞来源的皮肤疾病中提供持续的皮肤炎症反应。另外,治疗后bcl-2 +细胞的减少可能代表中等剂量UVA1光疗的关键机制。

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