Background: A dysregulated immune response has been implicated in Sweet syndrome (SS) pathogenesis; however, cytokine profiles across different conditions associated with SS - including adult-onset immunodeficiency (AOID) due to anti-interferon (IFN)-γ autoantibodies - remain unknown.
Objective: To investigate alterations in inflammatory cytokines in skin lesions of distinct subtypes of SS.
Methods: Skin biopsies were collected from 42 AOID- and 52 non-AOID-associated SS patients and 18 healthy controls. The comparative immunohistochemical study was conducted using monoclonal antibodies against interleukin (IL)-1β, IL-6, IL-17, IFN-γ, and tumor necrosis factor-α on paraffin-embedded sections. The quantitative percentage positivity and intensity were calculated using computer-based image analysis.
Results: The results showed stronger and more diffuse dermal immunoreactivity for IFN-γ and IL-17 in the AOID-associated ( < 0.001 and < 0.001, respectively) and non-AOID-associated SS ( < 0.001 and < 0.001, respectively) groups. However, no significant differences in the levels of these two cytokines were observed between the AOID- and non-AOID-associated SS groups. Increased expression of IFN-γ together with IL-17 was also noted in almost all subtypes among non-AOID-associated SS.
Conclusions: These results demonstrate that IFN-γ and IL-17 are implicated in immunopathology of all SS subtypes, including AOID-associated SS, despite the presence of anti-IFN-γ autoantibodies.
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http://dx.doi.org/10.3389/fimmu.2024.1355681 | DOI Listing |
Biomaterials
January 2025
Department of Pharmacy, Personalized Drug Therapy Key Laboratory of Sichuan Province, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China. Electronic address:
The chronic inflammation and matrix metalloprotease (MMP)-induced tissue degradation significantly disrupt re-epithelization and delay the healing process of diabetic wounds. To address these issues, we produced nanofibrils from Antheraea pernyi (Ap) silk fibers via a facile and green treatment of swelling and shearing. The integrin receptors on the cytomembrane could specifically bind to the Ap nanofibrils (ApNFs) due to their inherent Arg-Gly-Asp (RGD) motifs, which activated platelets to accelerate coagulation and promoted fibroblast migration, adhesion and spreading.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Medicine, Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Aurora, CO, USA.
Programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) interactions are targets for immunotherapies aimed to reinvigorate T cell function. Recently, it was documented that PD-L1 regulates dendritic cell (DC) migration through intracellular signaling events. In this study, we find that both preclinical murine and clinically available human PD-L1 antibodies limit DC migration.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
February 2025
Department of Urology and Andrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Cancer-associated fibroblasts (CAFs) are key stroma cells that play dominant roles in the migration and invasion of several types of cancer through the secretion of inflammatory cytokine IL-17A. This study aims to identify the potential role and regulatory mechanism of CAFs-secreted IL-17A in the migration and invasion of prostate cancer (PC). CAFs and normal fibroblasts (NFs) were obtained from fresh PC and its adjacent normal tissues, respectively.
View Article and Find Full Text PDFAllergy
January 2025
Department of Rheumatology and Immunology, University Hospital Bern, Inselspital, University of Bern, Bern, Switzerland.
Heliyon
January 2025
Guangdong Provincial Biotechnology Research Institute (Guangdong Provincial Laboratory Animals Monitoring Center), Guangzhou, Guangdong, 510663, China.
Spondyloarthritis is a prevalent and persistent condition that significantly impacts the quality of life. Its intricate pathological mechanisms have led to a scarcity of animal models capable of replicating the disease progression in humans, making it a prominent area of research interest in the field. To delve into the pathological and physiological traits of spontaneous non-human primate spondyloarthritis, this study meticulously examined the disease features of this natural disease model through an array of techniques including X-ray imaging, MRI imaging, blood biochemistry, markers of bone metabolism, transcriptomics, proteomics, and metabolomics.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!