Diversity of NF-κB signalling and inflammatory heterogeneity in Rheumatic Autoimmune Disease

Elsevier

Available online 3 September 2022, 101649

Seminars in ImmunologyHighlights•

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.

Abstract

Systemic 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.

Keywords

NF-κB

Systemic Autoimmune Rheumatic Diseases

Genetics

Rheumatoid Arthritis

Systemic Lupus Erythematosus

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© 2022 Published by Elsevier Ltd.

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