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Ulcerative colitis (UC) is a chronic relapsing disorder of the colonic tract, characterized by a dysregulated innate and adaptive immune response to gut microbiota that contributes to the perpetuation of intestinal inflammatory processes. The Interleukin (IL) 23/IL17 axis has been reported to play a key role in UC pathogenesis promoting Th17 cells and cytokines-related immune response. Recently, the blockade of IL23/IL17 pathways has been raised enormous interest in the treatment o several chronic inflammatory disorders. In this review, we summarize the emerging results from clinical trials that evoked both promise and discouragement in IL23/IL17 axis in the treatment of UC. Targeting IL23 p40 through Ustekinumab results safe and effective to induce and maintain clinical remission, low inflammatory indexes, mucosal healing, and a better quality of life. Studies targeting IL23 p19 through Mirikizumab, Risankizumab, Brazikumab and Guselkumab are still ongoing. To date, no clinical studies targeting IL17 pathway are ongoing in UC. IL-17 targeting is thought to have a context-dependent biological effect, based on whether cytokine is selectively targeted or if its function is dampened by the upstream block of IL23.
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http://dx.doi.org/10.3389/fimmu.2021.611256 | DOI Listing |
Br J Anaesth
September 2025
Department of Anesthesiology, the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China; Department of Pain Management, the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China. Electronic address: 45285184@qq
Biochim Biophys Acta Mol Basis Dis
September 2025
Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, China; State Key Laboratory of Frigid Zone Cardiovascular Disease, Harbin, 150086, Heilongjiang, China; The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry
Background And Aims: Viral myocarditis is an inflammatory pathology of the myocardium that involves innate immune responses, especially those involving neutrophils. However, strategies targeting neutrophils to alleviate inflammation have not achieved complete success. Alpha lipoic acid (ALA), a natural organosulfur compound, has the capacity to modulate immune cell behavior.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China; The Public Experimental Center of Medicine, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China. Electronic address: kexixian@z
Chemotherapy resistance in lung adenocarcinoma (LUAD) limits clinical efficacy. In this study, we first established circ_IGF2BP1 knockdown models in LUAD cells (A549 and H1299). Using dual-luciferase reporter assays, functional analyses, and miR-885-3p rescue experiments, we demonstrated that circ_IGF2BP1 promotes LUAD cell proliferation, migration, and invasion by directly targeting miR-885-3p.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Medical Center of Burn Plastic and Wound Repair, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi, China. Electronic address:
Skin scar formation is a critical pathological process in wound healing, but its underlying regulatory mechanisms remain incompletely elucidated. By integrating analyses of Bulk-RNA seq and single-cell RNA sequencing (scRNA-seq) data, we identified that ferroptosis-related biological processes potentially play a key role in skin scar formation. Further mechanistic studies demonstrated that in human dermal fibroblast cells, the ferroptosis regulator TIMP metallopeptidase inhibitor 1 (TIMP1) significantly promotes fibroblast differentiation toward a mature phenotype through interactions with cystatin C (CST3), characterized by upregulated expression of myofibroblast differentiation markers such as α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF), along with enhanced cell proliferation and migration abilities.
View Article and Find Full Text PDFJ Pharmacol Exp Ther
July 2025
Department of Pharmacy Practice, Parul Institute of Pharmacy & Research, Parul University, Limda, Waghodia, Vadodara, Gujarat, India. Electronic address:
Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by widespread inflammation and immune system dysregulation. Recent research suggests that the gut microbiota may play a role in the development of SLE by modulating immune system responses, affecting cytokine production, and altering the activity of T and B cells lymphocytes. As a result, there is a growing interest in microbiota-targeted therapies, including probiotics, dietary changes, and fecal microbiota transplantation.
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