Autoantigen TRIM21/Ro52 is expressed on the surface of antigen-presenting cells and its enhanced expression in Sjögren’s syndrome is associated with B cell hyperactivity and type I interferon activity
Author:
Publisher
BMJ
Subject
Immunology,Immunology and Allergy,Rheumatology
Reference11 articles.
1. Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23–Th17 pathway
2. Intracellular antibody-bound pathogens stimulate immune signaling via the Fc receptor TRIM21
3. Translocalized IgA mediates neutralization and stimulates innate immunity inside infected cells
4. Defects in lysosomal maturation facilitate the activation of innate sensors in systemic lupus erythematosus
5. Interaction between innate immunity and Ro52-induced antibody causes Sjögren's syndrome-like disorder in mice
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1. Roles of TRIM21/Ro52 in connective tissue disease-associated interstitial lung diseases;Frontiers in Immunology;2024-08-06
2. Reconstruction of Sjögren's syndrome-like sialadenitis by a defined disease specific gut-reactive single TCR and an autoantibody;Clinical Immunology;2024-07
3. The interconnected roles of TRIM21/Ro52 in systemic lupus erythematosus, primary Sjögren’s syndrome, cancers, and cancer metabolism;Cancer Cell International;2023-11-22
4. A Interacting Model: How TRIM21 Orchestrates with Proteins in Intracellular Immunity;Small Methods;2023-11-03
5. TRIM21 mediates the synergistic effect of Olaparib and Sorafenib by degrading BRCA1 through ubiquitination in TNBC;npj Breast Cancer;2023-10-20
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