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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
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Journey of B Cell Dysregulation in Rheumatoid Arthritis: Insights from Immunogenomics
Kabeer Haneef1,2, Muhammad Saleem Iqbal Khan3, Muhammad Umer Asghar4,5
1Department of Neuroscience, Chinese Institute for Brain Research (CIBR), Beijing, China.
Background:
Rheumatoid arthritis (RA) is a chronic autoimmune manifestation characterized by persistent chronic inflammation and joint damage. B cells play pivotal roles in the immune system, recognize antigens, and facilitate subsequent immune responses. Recent advancements in single-cell resolution techniques and immunogenomics have provided unprecedented insights into deciphering the complex mechanisms underlying B-cell dysregulation in RA.
Methods And Results:
This review article aims to articulate the current knowledge on how aberrant B cell activation and BCR signalling contribute to the development and perpetuation of self-reactive B cells in RA. Furthermore, this article explores immunogenomic insights that have shed light on the impaired B cell expansion and genetic variations in B cell-specific genes observed in RA patients, unveiling new layers of complexity in the underlying mechanisms driving autoimmune processes.
Conclusion:
This article focused on abberant B cell activation and immunogenomics aspects of B cells in rheumatoid arthritis. Precise identification of abberant BCR signalling pathways, abberant genetic variats and extensive abnormalities in DNA can provide detailed insights to direct structural and therapeutic interventions against autoimmune and hypersensitive disorders.
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