Currently, multiple studies have indicated that CD8+ T lymphocytes play a role in causing damage to the exocrine glands through acinar injury in primary Sjögren's syndrome (pSS). The aim of this research was to assess the imbalance of circulating CD8+ T cell subsets. We analyzed blood samples from 34 pSS patients and 34 healthy individuals as controls. We used flow cytometry to enumerate CD8+ T cell maturation stages, using as markers CD62L, CD28, CD27, CD4, CD8, CD3, CD45RA and CD45. For immunophenotyping of 'polarized' CD8+ T cell subsets, we used the following monoclonal antibodies: CXCR5, CCR6, CXCR3 and CCR4. The findings revealed that both the relative and absolute numbers of 'naïve' CD8+ T cells were higher in pSS patients compared to the healthy volunteers. Conversely, the proportions of effector memory CD8+ T cells were notably lower. Furthermore, our data suggested that among patients with pSS, the levels of cytotoxic Tc1 CD8+ T cells were reduced, while the frequencies of regulatory cytokine-producing Tc2 and Tc17 CD8+ T cells were significantly elevated. Simultaneously, the Tc1 cell subsets displayed a negative correlation with immunoglobulin G, rheumatoid factor, the Schirmer test and unstimulated saliva flow. On the other hand, the Tc2 cell subsets exhibited a positive correlation with these parameters. In summary, our study indicated that immune dysfunction within CD8+ T cells, including alterations in Tc1 cells, plays a significant role in the development of pSS.
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http://dx.doi.org/10.3390/biomedicines11102778 | DOI Listing |
Mol Cancer
December 2024
Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.
Cancer-associated fibroblasts (CAFs) exert multiple tumor-promoting functions and are key contributors to drug resistance. The mechanisms by which specific subsets of CAFs facilitate oxaliplatin resistance in colorectal cancer (CRC) have not been fully explored. This study found that THBS2 is positively associated with CAF activation, epithelial-mesenchymal transition (EMT), and chemoresistance at the pan-cancer level.
View Article and Find Full Text PDFTrends Immunol
December 2024
Heidelberg University, Medical Faculty Heidelberg, Department of Dermatology and National Center for Tumor Diseases (NCT), NCT Heidelberg, a partnership between DKFZ and University Hospital Heidelberg, Heidelberg, Germany; German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ) Core Center Heidelberg, 69120 Heidelberg, Germany. Electronic address:
Immune checkpoint inhibitors (ICIs) have transformed cancer treatment but are frequently associated with immune-related adverse events (irAEs). This article offers a novel synthesis of findings from both preclinical and clinical studies, focusing on the molecular mechanisms driving irAEs across diverse organ systems. It examines key immune cells, such as T cell subsets and myeloid cells, which are instrumental in irAE pathogenesis, alongside an in-depth analysis of cytokine signaling [interleukin (IL)-6, IL-17, IL-4), interferon γ (IFN-γ), IL-1β, tumor necrosis factor α (TNF-α)], integrin-mediated interactions [integrin subunits αITGA)4 and ITGB7], and microbiome-related factors that contribute to irAE pathology.
View Article and Find Full Text PDFJ Adv Res
December 2024
Department of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Institute of Digestive Disease, Inflammatory Bowel Disease Research Center, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Division of Gastroenterology and Hepatology, Baoshan Branch, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. Electronic address:
Introduction: In Crohn's disease (CD), lesions are mainly distributed in a segmental manner, with the primary sites of involvement being the ileum and colon. Heterogeneity in colon and ileum results in location-specific clinical presentations and therapeutic responses. Mucosal healing tends to be more readily and quickly achieved in the colon than in the ileum, where lesions are more likely to develop into complex behaviors.
View Article and Find Full Text PDFImmunity
December 2024
Division of Hematology/Oncology, Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA; Immunology Graduate Group, University of Pennsylvania, Philadelphia, PA, USA; Division of Hematologic Malignancies, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. Electronic address:
Innate-like splenic marginal zone (MZ) B (MZB) cells play unique roles in immunity due to their rapid responsiveness to blood-borne microbes. How MZB cells integrate cell-extrinsic and -intrinsic processes to achieve accelerated responsiveness is unclear. We found that Delta-like1 (Dll1) Notch ligands in splenic fibroblasts regulated MZB cell pool size, migration, and function.
View Article and Find Full Text PDFCurr Rheumatol Rep
December 2024
Department of Medicine, Division of Rheumatology, Queen's University, Kingston, ON, Canada.
Purpose Of Review: The canonical pathogenesis of spondyloarthritis (SpA) involves inflammation driven by HLA-B27, type 3 immunity, and gut microbial dysregulation. This review based on information presented at the SPARTAN meeting highlights studies on the pathogenesis of SpA from the past year, focusing on emerging mechanisms such as the roles of microbe-derived metabolites, microRNAs (miRNAs) and cytokines in plasma exosomes, specific T cell subsets, and neutrophils.
Recent Findings: The induction of arthritis in a preclinical model through microbiota-driven alterations in tryptophan catabolism provides new insights as to how intestinal dysbiosis may activate disease via the gut-joint axis.
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