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5-Aminolevulinic acid photodynamic therapy with and without Er:YAG laser for actinic keratosis: Changes in immune infiltration

机译:5-氨基乙酰丙酸光动力疗法联合或不联合Er:YAG激光治疗光化性角化病:免疫浸润的变化

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Introduction: Ultraviolet light induced DNA damage, combined with immunosuppression and inflammation are involved in the pathogenesis of actinic keratosis. Photodynamic therapy not only destroys dysplastic cells via tissue destruction and vascular shutdown, but also induces an acute local inflammatory response and activates both the innate and adaptive immune system. In our current work we aimed to compare immunohistochemistry features of inflammatory infiltrate of actinic keratoses after 5-aminolevulinic acid photodynamic therapy with or without Er:YAG laser resurfacing.Methods: Eleven patients with multiple actinic keratosis on the scalp, face, hands or forearms were treated by conventional and Er:YAG laser assisted 5-aminolevulinic acid PDT in split-site manner. Biopsies of AKs were taken before, 48 h and 3 months after the treatment. CD3, CD4, CD8, CD1a, Ki67 and p53 expressions were analyzed by immunohistochemical methods.Results: The number of p53 and Ki67 positive cells decreased significantly 3 months after treatment, but the abnormal cells were not eliminated totally. The number of CD1a Langerhans cells significantly decreased 48 h after both treatments, while CD8(+) T cell count was significantly lower 3 months after Er:YAG laser assisted photodynamic therapy. However, the number of CD3(+) and CD4(+) T cells were not changed significantly 48 h and 3 months later.Conclusions: One session of 5-aminolevulinic acid photodynamic therapy even with Er:YAG laser pretreatment could not terminate actinic damage totally. Photodynamic therapy induced immunological changes. However further investigations are needed to answer how the composition of actinic keratosis' immune infiltrate influence the effect of photodynamic therapy.
机译:简介:紫外线引起的DNA损伤,加上免疫抑制和炎症,都与光化性角化病的发病机理有关。光动力疗法不仅可以通过破坏组织和关闭血管来破坏增生细胞,还可以引起急性局部炎症反应,并激活先天和适应性免疫系统。在我们目前的工作中,我们旨在比较5-氨基乙酰丙酸光动力治疗与有或无Er:YAG激光重铺后光化性角化病的炎症浸润的免疫组织化学特征。方法:对11例头皮,面部,手或前臂多发性光化性角化病患者进行了研究。常规和Er:YAG激光辅助治疗的5-氨基乙酰丙酸PDT分部位治疗。在治疗前,治疗后48小时和3个月对AK进行活检。结果:用药3个月后,p53和Ki67阳性细胞明显减少,但异常细胞并未完全清除。两种治疗后48小时,CD1a Langerhans细胞的数量显着减少,而Er:YAG激光辅助光动力治疗3个月后,CD8(+)T细胞计数显着降低。然而,CD3(+)和CD4(+)T细胞的数目在48小时和3个月后没有明显改变。完全。光动力疗法引起免疫学改变。然而,需要进一步的研究来回答光化性角化病的免疫浸润成分如何影响光动力疗法的效果。

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