Elimination of B cells producing autoantibodies to neuroantigens is considered as beneficial in the treatment of multiple sclerosis. Myelin oligodendrocyte glycoprotein (MOG) is a significant autoantigen in multiple sclerosis. It was shown that MOG-like peptoid AMogP3 can bind autoantibodies produced by pathological lymphocytes. We propose a structure of an innovative drug for targeted elimination of the pool of autoreactive B cells responsible for multiple sclerosis pathogenesis; this compound is a complex of peptoid AMogP3 with Fc fragment of human immunoglobulin. The obtained Fc-PEG-AMogP3 conjugate effectively interact with autoreactive antibodies, which attests to their high therapeutic potential.
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http://dx.doi.org/10.1007/s10517-017-3711-4 | DOI Listing |
Mult Scler Relat Disord
January 2025
Multiple Sclerosis Center of Excellence West, Veterans Affairs, USA; Rehabilitation Care Service, VA Puget Sound Health Care System, 1660 S Columbian Way, Seattle, Washington, 98108, USA; Department of Rehabilitation Medicine, University of Washington, 325 9th Avenue, Seattle, Washington, 98104, USA. Electronic address:
Background/objective: Identifying research priorities of Veterans, MS researchers, and key stakeholders is critical to advance high-quality, evidence-based, and Veteran-specific MS care.
Methods: We used a modified Delphi approach to identify research priorities for Veterans with MS. Electronic surveys were distributed to Veterans with MS (n = 50,975), MS researchers (n = 191), VA healthcare providers (1,337), and funding agency representatives (n = 6) asking about their 2-3 most important research questions that would benefit Veterans with MS for researchers to answer in the next 5-10 years.
Clin Immunol
January 2025
Department of Pediatric Surgery, Children's Hospital of Fudan University, Shanghai Key Laboratory of Birth Defect, and Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai 201102, China. Electronic address:
The imbalance between Tregs and proinflammatory Th17 cells in children with biliary atresia (BA) causes immune damage to cholangiocytes. Dimethyl fumarate (DMF), an immunomodulatory drug, regulates the Treg/Th17 balance in diseases like multiple sclerosis (MS). This study explores DMF's effect on Treg/Th17 balance in BA and its potential mechanism.
View Article and Find Full Text PDFLancet Neurol
February 2025
Department of Neurology, International University of Health and Welfare, Narita, Japan.
Background: Evidence from preclinical studies suggests that IL-6 signalling has the potential to modulate immunopathogenic mechanisms upstream of autoantibody effector mechanisms in patients with generalised myasthenia gravis. We aimed to assess the safety and efficacy of satralizumab, a humanised monoclonal antibody targeting the IL-6 receptor, in patients with generalised myasthenia gravis.
Methods: LUMINESCE was a randomised, double-blind, placebo-controlled, multicentre, phase 3 study at 105 sites, including hospitals and clinics, globally.
Biomed Pharmacother
January 2025
Joseph Maxwell Cleland Atlanta VA Medical Center, Decatur, GA 30033, USA; Department of Orthopaedics, Emory Musculoskeletal Institute, Emory University, Atlanta, GA 30329, USA. Electronic address:
There is currently no cure or disease-modifying treatment for post-traumatic osteoarthritis (PTOA). This study aims to assess the efficacy of dimethyl fumarate (DMF), a US-FDA approved drug for multiple sclerosis, as a treatment for PTOA. PTOA was induced in male Lewis rats by medial meniscal transection (MMT) surgery, and DMF was intra-articularly administered once, one week following surgery.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
The First College of Clinical Medical Science, China Three Gorges University, 443000 Yichang, Hubei, China.
Multiple sclerosis (MS) is a chronic autoimmune disorder marked by neuroinflammation, demyelination, and neuronal damage. Recent advancements highlight a novel interaction between iron-dependent cell death, known as ferroptosis, and gut microbiota, which may significantly influences the pathophysiology of MS. Ferroptosis, driven by lipid peroxidation and tightly linked to iron metabolism, is a pivotal contributor to the oxidative stress observed in MS.
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