Available online 3 September 2022, 101649
Highlights•NF-κB-related genetic variants have been identified in most Systemic Autoimmune Rheumatic Diseases.
•Dysregulated NF-κB is present in most SARDs.
•Cell-specific NF-κB dysregulation may influence the site of inflammation.
•Cell- and pathway-specific NF-κB activity corresponds with RA synovial pathotypes.
AbstractSystemic Autoimmune Rheumatic Diseases, including Rheumatoid Arthritis, Systemic Lupus Erythematosus and Sjogren’s syndrome, are characterised by a loss of immune tolerance and chronic inflammation. There is marked heterogeneity in clinical and molecular phenotypes in each condition, and the aetiology of these is unclear. NF-κB is an inducible transcription factor that is critical in the physiological inflammatory response, and which has been implicated in chronic inflammation. Genome-wide association studies have linked risk alleles related to the NF-κB pathway to the pathogenesis of multiple Systemic Autoimmune Rheumatic Diseases. This review describes how cell- and pathway-specific NF-κB activation contribute to the spectrum of clinical phenotypes and molecular pathotypes in rheumatic disease. Potential clinical applications are explored, including therapeutic interventions and utilisation of NF-κB as a biomarker of disease subtypes and treatment response.
KeywordsNF-κB
Systemic Autoimmune Rheumatic Diseases
Genetics
Rheumatoid Arthritis
Systemic Lupus Erythematosus
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