Determination of T-cell clonality and expression profiles of Toll-like receptors signaling pathway genes and related miRNAs in patients with mycosis fungoides
Küçük Resim Yok
Tarih
2024
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Elsevier B.V.
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Cutaneous T-cell lymphomas (CTCL) encompass a group of diseases characterized by the presence of malignant clonal CD4+ T lymphocytes in the skin. Mycosis fungoides (MF) is the most prevalent form of CTCL, accounting for approximately 60 % of cutaneous T-cell lymphomas and 50 % of all primary cutaneous lymphomas. Despite ongoing research, the precise pathogenesis of MF remains incompletely understood. Toll-like receptors (TLRs) have the ability to specifically recognize ligands, subsequently induce the expression of diverse genes and activate innate immunity within the cell. Furthermore, miRNAs play a crucial role in regulating various aspects of immune cell function. The aim of our study was to explore the potential roles of TLRs and the genes implicated in their signal transduction, along with the expression status of miRNAs in the mechanisms underlying MF. Additionally, we assessed the clonal status and compared it with clinicopathological data using a T-cell clonality assay. To determine the expression status of TLR pathway genes and miRNAs, we conducted RT-PCR analysis on 52 MF samples and 50 control paraffin block materials. Pathway analysis were conducted using the KEGG database. T-cell receptor (TCR) gamma clonality changes were evaluated. Results from the study revealed increased expressions of TLR-1, -4, -8, IRF7, TRAF3, MEK1, MEK2, Elk1, NFkB, hsa-miR-21-5p, and hsa-miR-155-5p, as well as decreased expressions of hsa-miR-130a-3p, hsa-miR-210-3p, and hsa-let-7e-5p in the MF group. TCR gamma clonal change analysis demonstrated that 55.5 % of the analysed DNAs exhibited monoclonal and biallelic patterns, while 45.5 % displayed polyclonality. These findings collectively suggest the potential influence and therapeutic possibilities of the TLR signalling pathway in the molecular pathogenesis of MF. © 2023 Elsevier B.V.
Açıklama
Anahtar Kelimeler
Clonality, miRNAs, Mycosis fungoides, Toll-like receptors, DNA, immunoglobulin enhancer binding protein, interferon regulatory factor 7, microRNA, microRNA 130a 3p, microRNA 146a 5p, microRNA 155, microRNA 155 5p, microRNA 200a 3p, microRNA 204 5p, microRNA 21, microRNA 21 5p, microRNA 210 3p, microRNA 214 3p, microRNA 223 3p, microRNA 224 5p, microRNA 375, microRNA 424 5p, microRNA let 7e 5p, mitogen activated protein kinase kinase 1, mitogen activated protein kinase kinase 2, paraffin, toll like receptor, toll like receptor 1, toll like receptor 4, toll like receptor 8, transcription factor Elk 1, tumor necrosis factor receptor associated factor 3, unclassified drug, adolescent, adult, aged, allele, Article, child, clonal variation, controlled study, DNA determination, Elk1 gene, ERK1 gene, ERK2 gene, female, gene expression, gene function, histopathology, human, human cell, human tissue, infant, IRAK 4 gene, IRAK1 gene, IRF 7 gene, KEGG, major clinical study, male, MEK1 gene, MEK2 gene, molecular pathology, mycosis fungoides, MyD88 gene, NfkappaB gene, pathway analysis, protein expression, protein function, real time polymerase chain reaction, signal transduction, T lymphocyte, TAB2 gene, TIRAP gene, TLR 1 gene, TLR 10 gene, TLR 2 gene, TLR 3 gene, TLR 4 gene, TLR 5 gene, TLR 6 gene, TLR 7 gene, TLR 8 gene, TLR 9 gene, TLR gene, TLR signaling, TRAF 3 gene, TRAF 6 gene, TRIF gene, very elderly
Kaynak
Gene
WoS Q Değeri
Scopus Q Değeri
Q2
Cilt
891
