Designing mimetic of the interface functional groups of known receptor-ligand complexes is an attractive strategy for developing potential therapeutic agents that interfere with target protein-protein interactions. The CD80/CD86-CD28/CD152 costimulatory interactions transmit signals for CD4(+) T cell activation and suppression and are critically involved in the initiation, progression, and reactivation of the immunopathology in multiple sclerosis. Differences in the pattern, levels, and kinetics of expression of CD80/CD86 molecules in conjunction with differences in the strength of the signals delivered upon binding CD28 or CD152 determine the outcome of the immune response. A temporal up-regulation of surface expression of CD80 relative to CD86 on APCs and CNS-infiltrating cells has been shown to correlate with disease progression in experimental autoimmune encephalomyelitis an animal model for multiple sclerosis. Hence blockade of the CD80 costimulatory axis has therapeutic potential in multiple sclerosis. In this study, we report the efficacy of a novel CD80-blocking agent CD80-competitive antagonist peptide (CD80-CAP) in suppressing clinical disease and relapse in experimental autoimmune encephalomyelitis. The CD80-CAP mediates protection by inhibiting proinflammatory cytokines and skewing toward anti-inflammatory response presumably by enhancing the expression of glucocorticoid-induced leucine zipper in activated CD4(+) T cells.
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http://dx.doi.org/10.4049/jimmunol.0902056 | DOI Listing |
Oligodendroglial lineage cells (OLCs) are critical for neuronal support functions, including myelination and remyelination. Emerging evidence reveals their active roles in neuroinflammation, particularly in conditions like Multiple Sclerosis (MS). This study explores the inflammatory translatome of OLCs during the early onset of experimental autoimmune encephalomyelitis (EAE), an established MS model.
View Article and Find Full Text PDFCommun Biol
January 2025
Department of Medicine, Universite de Montreal, Montreal, QC, Canada.
Severe COVID-19 can trigger a cytokine storm, leading to acute respiratory distress syndrome (ARDS) with similarities to superantigen-induced toxic shock syndrome. An outstanding question is whether SARS-CoV-2 protein sequences can directly induce inflammatory responses. In this study, we identify a region in the SARS-CoV-2 S2 spike protein with sequence homology to bacterial super-antigens (termed P3).
View Article and Find Full Text PDFJ Community Genet
January 2025
Centralized Sequencing Program, National Institute of Allergy and Infectious Diseases (NIAID), Bethesda, MD, USA.
Inborn errors of immunity (IEI) are rare heritable disorders of the immune system predisposing to atypical infections, autoimmunity, inflammation, and risk of malignancy. Adaptation is the process of incorporating stressful experiences into one's life; these experiences may include onset of illness, receiving a diagnosis, or suffering without a diagnosis. Poor adaptation is linked to adverse outcomes including psychiatric comorbidities and decreased well-being.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
January 2025
Department of Experimental Medicine, Sapienza University of Rome, Italy.
Context: Autoantibodies against IFN-α (AAb-IFN-α) might be associated with the less aggressive autoimmunity in latent autoimmune diabetes in adults (LADA) compared to early-onset type 1 diabetes (T1D).
Objective: To investigate the presence and clinical relevance of the positivity to AAb-IFN-α in people with LADA compared to T1D.
Research Design And Methods: Serum levels of AAb against IFN-α isoforms were measured using a cell-based approach in 41 subjects with LADA and in 90 subjects with T1D.
Lancet Reg Health Eur
February 2025
Institute of Medical Immunology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Augustenburger Platz 1, Berlin, 13353, Germany.
Background: Since the pandemic, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become the leading trigger for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Evidence indicates that autoimmunity plays an important pathophysiological role. We aimed to evaluate the effectiveness of IA treatment in post-COVID ME/CFS patients.
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