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Pathogenesis of rheumatoid arthritis: one year in review 2026

1, 2, 3, 4, 5, 6, 7

 

  1. Immuno-Allergology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy.
  2. Immuno-Allergology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy.
  3. Immuno-Allergology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy.
  4. University of L’Aquila, Department of Life, Health & Environmental Sciences, Division of Internal Medicine and Nephrology, ASL 1 Avezzano-Sulmona, L’Aquila, San Salvatore Hospital, L’Aquila, Italy.
  5. Immuno-Allergology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy.
  6. University of L’Aquila, Department of Life, Health & Environmental Sciences, Division of Internal Medicine and Nephrology, ASL 1 Avezzano-Sulmona, L’Aquila, San Salvatore Hospital, L’Aquila, Italy.
  7. Immuno-Allergology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Italy. ilaria.puxeddu@unipi.it

CER20284
2026 Vol.44, N°9
PI 1691, PF 1696
Review

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Received: 01/07/2026
Accepted : 03/09/2026
In Press: 08/09/2026
Published: 08/09/2026

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterised by joint destruction and extra-articular manifestations. It is well known that underlying the pathogenesis of the disease a complex interplay of genetic susceptibility, epigenetic modifications, and immune dysregulation takes place. Over the past year, basic and clinical research studies in the field of RA have been conducted, shedding further light on certain pathogenetic mechanisms not yet fully clarified. In particular, advances have been made in understanding the interaction between cells of the innate immune system, such as neutrophils and macrophages, and structural cells, such as fibroblast-like synoviocytes (FLS). Furthermore, due to recent findings obtained at cellular and molecular levels, it has been possible to better define the interactions between the innate and adaptive immune systems and to better explain how RA-specific antibodies can exert a regulatory effect on the innate immune system. Identifying new elements regulating the mechanisms underlying RA pathogenesis is crucial for designing new therapeutic strategies and utilising biomarkers useful for the diagnosis and managements of the disease.

Rheumatology Article