LEO Foundation Skin Immunology Research Center, Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.
Department of Pathology, Zealand University Hospital, Roskilde, Denmark; Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
J Invest Dermatol. 2021 Oct;141(10):2449-2458. doi: 10.1016/j.jid.2021.01.038. Epub 2021 Apr 20.
Staphylococcal enterotoxins are believed to fuel disease activity in cutaneous T-cell lymphoma. Recent data support this by showing that antibiotics inhibit malignant T cells in skin lesions in mycosis fungoides and Sézary syndrome, the most common forms of cutaneous T-cell lymphoma. Yet, it remains incompletely characterized how staphylococcal enterotoxins fuel disease activity. In this study, we show that staphylococcal enterotoxins induce the expression of the oncogenic microRNA miR-155 in primary malignant T cells. Thus, staphylococcal enterotoxins and Staphyloccocus aureus isolates from lesional skin of patients induce miR-155 expression at least partly through the IL-2Rg‒Jak‒signal transducer and activator of transcription 5 pathway, and the effect is augmented by the presence of nonmalignant T cells. Importantly, mycosis fungoides lesions harbor S. aureus, express Y-phosphorylated signal transducer and activator of transcription 5, and display enhanced miR-155 expression, when compared with nonlesional and healthy skin. Preliminary data show that aggressive antibiotic therapy is associated with decreased Y-phosphorylated signal transducer and activator of transcription 5 and miR-155 expression in lesional skin in two patients with Sézary syndrome. In conclusion, we show that S. aureus and its enterotoxins induce enhanced expression of oncogenic miR-155, providing mechanistic insight into the role of S. aureus in cutaneous T-cell lymphoma. Our findings support that environmental stimuli such as bacteria can fuel disease progression in cutaneous T-cell lymphoma.
葡萄球菌肠毒素被认为会引发皮肤 T 细胞淋巴瘤的疾病活动。最近的数据支持这一观点,表明抗生素可以抑制蕈样肉芽肿和塞扎里综合征(最常见的皮肤 T 细胞淋巴瘤形式)皮损中的恶性 T 细胞。然而,葡萄球菌肠毒素如何引发疾病活动仍不完全清楚。在这项研究中,我们表明葡萄球菌肠毒素可诱导原代恶性 T 细胞中致癌 microRNA miR-155 的表达。因此,葡萄球菌肠毒素和来自患者皮损皮肤的金黄色葡萄球菌分离株至少部分通过 IL-2Rg-Jak-信号转导和转录激活因子 5 途径诱导 miR-155 表达,并且非恶性 T 细胞的存在会增强这种作用。重要的是,与非皮损和健康皮肤相比,蕈样肉芽肿病变中存在金黄色葡萄球菌,表达 Y 磷酸化信号转导和转录激活因子 5,并显示增强的 miR-155 表达。初步数据表明,在两名塞扎里综合征患者中,侵袭性抗生素治疗与皮损中 Y 磷酸化信号转导和转录激活因子 5 和 miR-155 表达的降低相关。总之,我们表明金黄色葡萄球菌及其肠毒素可诱导致癌 miR-155 的表达增强,为金黄色葡萄球菌在皮肤 T 细胞淋巴瘤中的作用提供了机制上的见解。我们的发现支持这样一种观点,即环境刺激物(如细菌)可以促进皮肤 T 细胞淋巴瘤的疾病进展。