Air pollution as a determinant of rheumatoid arthritis

• Published in: Joint, bone, spine : revue du rhumatisme bone, spine : revue du rhumatisme, 2019-01, Vol.86 (1), p.37-42
• Main Authors: Sigaux, Johanna, Biton, Jérôme, André, Emma, Semerano, Luca, Boissier, Marie-Christophe
• Format: Article
• Language: English
• Subjects: Air pollution; Air Pollution - adverse effects; Air Pollution - statistics & numerical data; Animals; Anti-Citrullinated Protein Antibodies - biosynthesis; Anti-Citrullinated Protein Antibodies - immunology; Arthritis, Rheumatoid - epidemiology; Arthritis, Rheumatoid - etiology; Arthritis, Rheumatoid - immunology; Arthritis, Rheumatoid - physiopathology; Aryl hydrocarbon receptor; Autoimmune Diseases - epidemiology; Autoimmune Diseases - etiology; Autoimmune Diseases - immunology; Autoimmune Diseases - physiopathology; Autoimmunity; Basic Helix-Loop-Helix Transcription Factors - biosynthesis; Basic Helix-Loop-Helix Transcription Factors - immunology; Fine particles; Humans; Life Sciences; Lung - immunology; Lung - physiopathology; Mice; Particulate Matter - adverse effects; Particulate Matter - immunology; Receptors, Aryl Hydrocarbon - biosynthesis; Receptors, Aryl Hydrocarbon - immunology; Rheumatoid arthritis; Urban Population - statistics & numerical data
• ISSN: 1297-319X; 1778-7254
• DOI: 10.1016/j.jbspin.2018.03.001

•Residence in an urban area is associated with a higher incidence of RA, and living near an air pollution emitter site is associated with a higher risk of developing RA and producing ACPAs.•Histologically, tertiary lymphoid structures (inducible bronchus-associated lymphoid tissue or iBALT) act as a mediator linking particulate matter, citrullination, and RA.•At the cellular level, the aryl hydrocarbon receptor (AHR) links particulate matter, T-cell polarization, and RA. Pollution has long been incriminated in many cardiovascular and respiratory diseases. More recently, studies evaluated the potential role for particulate pollutants in autoimmune diseases, including rheumatoid arthritis (RA). The incidence of RA was found to be higher in urban areas. Living near air pollution emitters was associated with higher risks of developing RA and of producing RA-specific autoantibodies. Nevertheless, no strong epidemiological evidence exists to link one or more specific air pollution particles to RA. The presence in the bronchi of lymphoid satellite islands (inducible bronchus-associated lymphoid tissue, iBALT) is strongly associated with both inflammatory lung disease and RA-associated lung disease. Diesel exhaust particles can stimulate iBALT formation. The induction by air pollution of an inflammatory environment with high citrullination levels in the lung may induce iBALT formation, thereby causing a transition toward a more specific immune response via the production of anti-citrullinated peptide antibodies. Air pollution not only triggers innate immune responses at the molecular level, increasing the levels of proinflammatory cytokines and reactive oxygen species, but is also involved in adaptive immune responses. Thus, via the aryl hydrocarbon receptor (AHR), diesel exhaust particles can trigger a T-cell switch to the Th17 profile. Finally, in the murine collagen-induced arthritis model, animals whose lymphocytes lack the AHR develop milder arthritis.