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Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling
Published on: October 14, 2021
Pathogenesis of cutaneous T-cell lymphoma: Malignant inflammation, immune reprogramming, and microenvironmental
Joana Calvão1, Christoph Iselin2, Johannes Wasmayr2
1Dermatology Department of Coimbra University Hospital, Local Health Unit of Coimbra, Coimbra, Portugal; Faculty of Medicine of Coimbra University, Coimbra, Portugal.
Abstract:
Cutaneous T-cell lymphomas, namely mycosis fungoides and Sézary syndrome, arise through a complex interplay of genetic alterations, epigenetic deregulation, immune imbalance, and tumor-microenvironment interactions. A progressive T helper 1-to-T helper 2 shift and chemokine-directed trafficking promote immune evasion and sustained malignant T-cell activity, whereas emerging data show subclonal diversity enabling adaptation to microenvironmental and therapeutic pressures. Skin-resident immune cells further shape disease behavior, and Staphylococcus aureus superantigens act as microenvironmental amplifiers that enhance malignant signaling and contribute to treatment resistance. A deeper understanding of how these molecular, immunological, and microbiome factors converge is essential to develop more precise, biomarker-informed therapeutic strategies.
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