Background: One mechanism that underlies protection from autoimmunity and avoidance of uncontrolled inflammation is the controlled contraction of lymphocyte expansion during the immune response. We identified regulatory rheumatoid factor (regRF), the production of which is associated with resistance to and remission of experimental autoimmune diseases. RegRF is anti-idiotypic antibodies to lymphocyte receptors against autoimmune disease-inducing antigens; at the same time, it is specific to epitopes in the hinge Fc fragments of IgG.
Objective: The aim of this study is to test the hypothesis that regRF prevents autoimmunity by limiting the expansion of lymphocytes.
Methods: To test this hypothesis, we used a model of experimental autoimmune encephalitis.
Results: We found that in the lymph nodes that drain the injection site in rats producing regRF in response to immunization with myelin basic protein (MBP) the proportion of CD4+lymphocytes was lower than in rats in which MBP-immunization did not induce higher regRF levels. RegRF-containing plasma obtained from MBP-immunized rats induces complement-dependent killing of MBP-activated lymphocytes. Activated MBP-specific lymphocytes are not sensitive to the regRF-containing plasma of intact rats.
Conclusion: The regRF produced during the immune response is a specific control factor for the expansion of antigen-activated CD4+lymphocytes.
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http://dx.doi.org/10.2174/1871530318666180308123350 | 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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