皮肤 T 细胞淋巴瘤与微生物群:皮肤 T 细胞淋巴瘤与微生物群:发病机制和潜在的新治疗靶点》。

IF 1.5 Q3 DERMATOLOGY
Dermatology Research and Practice Pub Date : 2024-02-22 eCollection Date: 2024-01-01 DOI:10.1155/2024/9919225
Daniel Rodríguez Baeza, Lía Bejarano Antonio, Marta González de Arriba, José Antonio Picó-Monllor, Javier Cañueto, Vicente Navarro-Lopez
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引用次数: 0

摘要

目的回顾与人类微生物群和皮肤 T 细胞淋巴瘤相关的科学文献。方法:探索性和系统性综述从文献数据库 MEDLINE (PubMed)、Embase、The Cochrane Library 和 Scopus 中检索过去 10 年发表的文章,并使用以下描述符进行探索性和系统性综述:"淋巴瘤、T 细胞、皮肤"、"微生物群"、"真菌病"、"塞扎里综合征"、"淋巴瘤、原发性皮肤无性大细胞"、"淋巴瘤样乳头状瘤病 "以及 "微生物群"、"微生物群"、"微生物群落 "和 "微生物群落":在检索到的 87 篇参考文献中,按照纳入和排除标准筛选出 21 篇文章。大多数将皮肤 T 细胞淋巴瘤与微生物群联系起来的研究都侧重于皮肤微生物群,其中金黄色葡萄球菌是主要的相关病原体。这种细菌在皮肤上的定植可能与 STAT3 炎症通路的过度激活和 IL-17 的过度产生有关,而这两者都与更具侵袭性和晚期形式的皮肤 T 细胞淋巴瘤的发展广泛相关。我们还发现了肠道菌群失调与皮肤 T 细胞淋巴瘤发病之间可能存在关系的证据,观察到皮肤 T 细胞淋巴瘤患者肠道微生物组中的分类变异性降低,某些菌属如 Prevotella 增加。这种关系的可能致病机制可能是全身细胞因子释放增加,促进了皮肤水平的 STAT3 过度激活:结论:皮肤T细胞淋巴瘤与皮肤和肠道微生物组之间似乎存在某种关系,并可能涉及一种病理生理途径。在后一种情况下,使用药理学工具(如 JAK 抑制剂或 IL-17 抑制剂)对皮肤和肠道微生物组进行可能的调节或对信号炎症通路产生作用,可为未来皮肤 T 细胞淋巴瘤的治疗研究提供可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cutaneous T-Cell Lymphoma and Microbiota: Etiopathogenesis and Potential New Therapeutic Targets.

Objective: To review the scientific literature related to human microbiota and cutaneous T-cell lymphoma. Methodology. An exploratory and systematic review of the articles retrieved from the bibliographic databases MEDLINE (PubMed), Embase, The Cochrane Library, and Scopus, published in the last 10 years with the following descriptors: "lymphoma, T-cell, cutaneous," "microbiota," "Mycosis Fungoides," "Sézary Syndrome," "lymphoma, primary cutaneous anaplastic large cell," "Lymphomatoid Papulosis" and "Microbiota," "microbiota," "Microbial Community," and "Microbial Communities."

Results: Of the 87 references retrieved, after applying the inclusion and exclusion criteria, 21 articles were selected. Most studies linking cutaneous T-cell lymphoma and the microbiota focus on the cutaneous microbiome, with Staphylococcus aureus being the main related agent. Skin colonization by this bacterium could be involved in the hyperactivation of the STAT3 inflammatory pathway and in the overproduction of IL-17, both of which are widely related to the development of more aggressive and advanced forms of cutaneous T-cell lymphoma. We also found evidence of a possible relationship between intestinal dysbiosis and the development of cutaneous T-cell lymphoma, observing a decrease in taxonomic variability and an increase in certain genera such as Prevotella in the intestinal microbiome of patients with cutaneous T-cell lymphoma. The possible etiopathogenic mechanism underlying this relationship could be explained by an increase in systemic cytokine release, promoting the hyperactivation of STAT3 at the skin level.

Conclusion: There appears to be a relationship between cutaneous T-cell lymphoma and the cutaneous and intestinal microbiome, as well as a possible pathophysiological pathway involved. The possible modulation of the cutaneous and intestinal microbiome or the action on the signaling inflammatory pathway, using pharmacological tools such as JAK inhibitors or IL-17 inhibitors in the latter case, could open the possibility for future therapeutic studies for cutaneous T-cell lymphoma.

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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
16
审稿时长
11 weeks
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