2,884 results match your criteria: "Nature reviews. Rheumatology[Journal]"
Nat Rev Rheumatol
December 2024
Centre for Aging, Rheumatology and Regenerative Medicine, University College London, London, UK.
Nat Rev Rheumatol
December 2024
Nature Reviews Rheumatology, .
Nat Rev Rheumatol
December 2024
Nature Reviews Rheumatology, .
Nat Rev Rheumatol
December 2024
Division of Rheumatology & Clinical Immunology, University of Pittsburgh, Pittsburgh, PA, USA.
Nat Rev Rheumatol
December 2024
Department of Orthopedic Surgery, Surgical Science, Tokai University School of Medicine, Isehara, Japan.
Nat Rev Rheumatol
December 2024
Center for Translational Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA.
Antigen-specific therapies have a long history in the treatment of allergy but have not been successful in autoimmunity. However, in the past 20 years, advances in the definition of the self-antigens that promote autoimmunity and the growing understanding of the mechanisms that maintain tolerance in health but fail in autoimmunity have led to antigen-specific approaches being considered for the treatment of autoimmune diseases. The core goal of each antigen-specific treatment approach is to remove the immune response that promotes autoimmunity whilst sparing protective responses.
View Article and Find Full Text PDFNat Rev Rheumatol
December 2024
Nature Reviews Rheumatology, .
Nat Rev Rheumatol
December 2024
Department of Biological Sciences, College of Medicine and Health Sciences, Khalifa University, Abu Dhabi, United Arab Emirates.
Nat Rev Rheumatol
January 2025
Department of Medicine IV, Hospital of LMU Munich, Munich, Germany.
Nat Rev Rheumatol
January 2025
Division of Rheumatology, Inflammation, and Immunity, Brigham and Women's Hospital, Boston, MA, USA.
Classic regulatory T (T) cells expressing CD4 and the hallmark transcription factor FOXP3 are integral to the prevention of multi-system autoimmunity. However, immune-mediated arthritis is often associated with increased numbers of T cells in the inflamed joints. To understand these seemingly conflicting observations, which we collectively describe as 'the T paradox', we provide an overview of T cell biology with a focus on T cell heterogeneity, function and dysfunction in arthritis.
View Article and Find Full Text PDFNat Rev Rheumatol
January 2025
Nature Reviews Rheumatology, .
Nat Rev Rheumatol
January 2025
Nature Reviews Rheumatology, .
Nat Rev Rheumatol
December 2024
Pediatric Translational Research Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.
Nat Rev Rheumatol
January 2025
Translational Autoinflammatory Diseases Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Nat Rev Rheumatol
January 2025
GENYO Center for Genomics and Oncological Research, Pfizer-University of Granada-Andalusian Regional Government, Granada, Spain.
Nat Rev Rheumatol
January 2025
Department of Ageing, Rheumatology and Regenerative Medicine, Division of Medicine, University College London, London, UK.
Myositis-specific autoantibodies (MSAs) have become pivotal biomarkers for idiopathic inflammatory myopathies and have revolutionized understanding of the heterogeneous disease spectrum that affects both adults and children. The discovery and characterization of MSAs have substantially enhanced patient stratification based on clinical phenotype, thereby facilitating more precise diagnosis and ultimately improving management strategies. Advances in immunoassay technologies in the past 20 years have further propelled the field forward, enabling the detection of a growing repertoire of autoantibodies with high specificity and sensitivity; however, evolving research over the past decade has revealed that even within antibody-defined subsets, considerable clinical diversity exists, suggesting a broader spectrum of disease manifestations than previously acknowledged.
View Article and Find Full Text PDFNat Rev Rheumatol
November 2024
School of Infection and Immunity, University of Glasgow, Glasgow, UK.
Nat Rev Rheumatol
January 2025
Department of Rheumatology and Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Nat Rev Rheumatol
November 2024
Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Nat Rev Rheumatol
January 2025
Division of Rheumatology, Department of Medicine, Dalhousie University and Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia, Canada.
Nat Rev Rheumatol
December 2024
AMPEL BioSolutions, Charlottesville, VA, USA.
Emerging evidence indicates that memory B cells are dysfunctional in systemic lupus erythematosus (SLE). They are hyporesponsive to signalling through the B cell receptor (BCR) but retain responsiveness to Toll-like receptor (TLR) and type I interferon signalling, as well as to T cell-mediated activation via CD40-CD154. Chronic exposure to immune complexes of ribonucleoprotein (RNP)-specific autoantibodies and TLR-engaging or BCR-engaging cargo is likely to contribute to this partially anergic phenotype.
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