Rheumatoid arthritis (RA) is a common autoimmune disorder initiated by inflammatory synovitis. Hyperproliferation of destructive synovial fibroblasts (SFs) is one of the pathogenic mechanisms of RA. Abnormalities in regulatory T cells (Tregs) may also play a critical role in this progression. To date, it is unclear whether both natural Tregs (nTregs) and induced Tregs (iTregs) share similar characteristics in RA progression and whether Tregs directly suppress the autoaggressive activities of SFs. In this study, we compared suppressive effects on effector T cells (Teffs) and inflamed SFs between nTregs and iTregs in a collagen-induced arthritis (CIA) model. Our results demonstrated that iTregs but not nTregs maintained a suppressive effect on Teffs after adoptive transfer into CIA mice. Additionally, we discovered that iTregs directly inhibited the destructive activities of CIA-SFs. Thus, this study suggests that administration of the iTreg subset has great potential for treatment of RA in the clinic in the future.
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http://dx.doi.org/10.1007/s12026-023-09370-8 | DOI Listing |
Elife
January 2025
Instituto Gulbenkian de Ciência, Rua da Quinta Grande, Oeiras, Portugal.
During the trunk to tail transition the mammalian embryo builds the outlets for the intestinal and urogenital tracts, lays down the primordia for the hindlimb and external genitalia, and switches from the epiblast/primitive streak (PS) to the tail bud as the driver of axial extension. Genetic and molecular data indicate that Tgfbr1 is a key regulator of the trunk to tail transition. Tgfbr1 has been shown to control the switch of the neuromesodermal competent cells from the epiblast to the chordoneural hinge to generate the tail bud.
View Article and Find Full Text PDFAsian Pac J Cancer Prev
January 2025
Cancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, 55281 Yogyakarta, Indonesia.
Objective: Programmed cell death-1 (PD-1, encoded by PDCD1) regulatory network participates in glioblastoma multiforme development. However, such a network in trastuzumab-resistant human epidermal growth factor receptor 2-positive (HER2+) breast cancer remains to be determined. Accordingly, this study was aimed to explore the PD-1 regulatory network responsible for the resistance of breast cancer cells to trastuzumab through a bioinformatics approach.
View Article and Find Full Text PDFFASEB J
January 2025
State Key Laboratory of Swine and Poultry Breeding Industry, Sichuan Agricultural University, Chengdu, China.
Triglyceride (TG) metabolism is a complex and highly coordinated biological process regulated by a series of genes, and its dysregulation can lead to the occurrence of disorders in lipid metabolism. However, the transcriptional regulatory mechanisms of crucial genes in TG metabolism mediated by enhancer-promoter interactions remain elusive. Here, we identified candidate enhancers regulating the Agpat2, Dgat1, Dgat2, Pnpla2, and Lipe genes in 3T3-L1 adipocytes by integrating epigenomic data (H3K27ac, H3K4me1, and DHS-seq) with chromatin three-dimensional interaction data.
View Article and Find Full Text PDFCell Biol Toxicol
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Department of Oral Anatomy and Physiology, Hospital of Stomatology, Jilin Provincial Key Laboratory of Oral Biomedical Engineering, Jilin University, Changchun, 130021, China.
Novel strategies to disrupt tumor progression have emerged from studying the interactions between tumor cells and tumor-associated macrophages (TAMs). However, the molecular mechanisms of interactions between tumor cells and TAMs underlying oral squamous cell carcinoma (OSCC) progression have not been fully elucidated. This study explored the molecular mechanism of the HSP27/IL-6 axis in OSCC chemoresistance, invasion, and migration.
View Article and Find Full Text PDFJ Exp Med
March 2025
Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Activation of CD8+ T cells necessitates rapid metabolic reprogramming to fulfill the substantial biosynthetic demands of effector functions. However, the posttranscriptional mechanisms underpinning this process remain obscure. The transfer RNA (tRNA) N1-methyladenine (m1A) modification, essential for tRNA stability and protein translation, has an undefined physiological function in CD8+ T cells, particularly in antitumor responses.
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