Rodríguez Baeza Daniel, Bejarano Antonio Lía, González de Arriba Marta, Picó-Monllor José Antonio, Cañueto Javier, Navarro-Lopez Vicente
Dermatology Service, Rio Hortega University Hospital, Calle Dulzaina, 2, Valladolid 47012, Spain.
MiBioPath Research Group, Medicine Faculty, Catholic University of Murcia (UCAM), Av. de los Jerónimos, 135, Murcia 30107, Spain.
Dermatol Res Pract. 2024 Feb 22;2024:9919225. doi: 10.1155/2024/9919225. eCollection 2024.
To review the scientific literature related to human microbiota and cutaneous T-cell lymphoma. . 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."
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 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 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.
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.
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。对从MEDLINE(PubMed)、Embase、Cochrane图书馆和Scopus等文献数据库中检索到的文章进行探索性和系统性综述,这些文章发表于过去10年,使用了以下描述词:“淋巴瘤,T细胞,皮肤型”、“微生物群”、“蕈样肉芽肿”、“塞扎里综合征”、“原发性皮肤间变性大细胞淋巴瘤”、“淋巴瘤样丘疹病”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,应用纳入和排除标准后,选取了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聚焦于皮肤微生物组,[细菌名称]是主要相关因素。这种细菌在皮肤的定植可能参与STAT3炎症通路的过度激活以及IL - 17的过度产生,这两者都与更具侵袭性和晚期形式的皮肤T细胞淋巴瘤的发展密切相关。我们还发现肠道生态失调与皮肤T细胞淋巴瘤的发展之间可能存在关联的证据,观察到皮肤T细胞淋巴瘤患者肠道微生物组的分类变异性降低,某些菌属如[菌属名称]增加。这种关系背后可能的病因机制可以通过全身细胞因子释放增加来解释,从而促进皮肤水平的STAT3过度激活。
皮肤T细胞淋巴瘤与皮肤和肠道微生物组之间似乎存在关联,以及一条可能涉及的病理生理途径。使用JAK抑制剂等药物工具对皮肤和肠道微生物组进行可能的调节,或者在后一种情况下对炎症信号通路采取行动,可能为未来皮肤T细胞淋巴瘤的治疗研究开辟可能性。