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Crisdesalazine alleviates inflammation in an experimental autoimmune encephalomyelitis multiple sclerosis mouse model by regulating the immune system.
BMC Neurosci
January 2025
Laboratory of Veterinary Internal Medicine, Department of Clinical Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul, 08826, Republic of Korea.
Microglia/macrophages participate in the development of and recovery from experimental autoimmune encephalomyelitis (EAE), and the macrophage M1 (pro-inflammatory)/M2 (anti-inflammatory) phase transition is involved in EAE disease progression. We evaluated the efficacy of crisdesalazine (a novel microsomal prostaglandin E2 synthase-1 inhibitor) in an EAE model, including its immune-regulating potency in lipopolysaccharide-stimulated macrophages, and its neuroprotective effects in a macrophage-neuronal co-culture system. Crisdesalazine significantly alleviated clinical symptoms, inhibited inflammatory cell infiltration and demyelination in the spinal cord, and altered the phase of microglial/macrophage and regulatory T cells.
View Article and Find Full Text PDFQuantification of Citrullinated Histone H3 as a Marker for Neutrophil Extracellular Traps Correlated to Clinical Characteristics of Patients with Systemic Lupus Erythematosus.
Arch Immunol Ther Exp (Warsz)
January 2025
Department of Human Physiology, Medical University of Lublin, Lublin, Poland.
Systemic lupus erythematosus (SLE) is an autoimmune disease whose pathogenesis is not fully understood to date. One of the suggested mechanisms for its development is NETosis, which involves the release of a specific network consisting of chromatin, proteins, and enzymes from neutrophils, stimulating the immune system. One of its markers is citrullinated histone H3 (H3Cit).
View Article and Find Full Text PDFProfile and Usefulness of Serum Cytokines to Predict Prognosis in Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease.
Neurol Neuroimmunol Neuroinflamm
March 2025
Hospices Civils de Lyon, Service de Neurologie, Sclérose en Plaques, Pathologies de la Myéline et Neuro-Inflammation-Hôpital Neurologique Pierre Wertheimer, Bron Cedex.
Objectives: To characterize the serum cytokine profile in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) at onset and during follow-up and assess their utility for predicting relapses and disability.
Methods: This retrospective multicentric cohort study included patients aged 16 years and older meeting MOGAD 2023 criteria, with serum samples collected at baseline (≤3 months from disease onset) and follow-up (≥6 months from the baseline), and age-matched and time to sampling-matched patients with multiple sclerosis (MS). Eleven cytokines were assessed using the ELLA system.
Large-scale multicenter study reveals anticitrullinated SR-A peptide antibody as a biomarker and exacerbator for rheumatoid arthritis.
Sci Adv
January 2025
Department of Rheumatology and Immunology, Peking University People's Hospital & Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), Beijing, China.
Current diagnosis and treatment of rheumatoid arthritis (RA) is still challenging. More than one-third of patients with RA could not be accurately diagnosed because of lacking biomarkers. Our recent study reported that scavenger receptor-A (SR-A) is a biomarker for RA, especially for anticyclic citrullinated peptide antibody (anti-CCP)-negative RA.
View Article and Find Full Text PDFPtpA protein from Mycobacterium avium subsp. paratuberculosis as a potential marker of rheumatoid arthritis in humans.
PLoS One
January 2025
Instituto de Investigación en Ciencias Biomédicas, Centro Universitario de Ciencias de la Salud Universidad de Guadalajara, Guadalajara, Mexico.
Studies have noted the connection between Mycobacterium avium subspecies paratuberculosis (MAP) and autoimmunity. MAP is an intracellular pathogen that infects and multiplies in macrophages. To overcome the hostile environment elicited by the macrophage, MAP secretes a battery of virulence factors to neutralize the toxic effects of the macrophage.
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