Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease caused by both genetic and environmental factors. Smoking has been implicated as one of the most important extrinsic risk factors for its development and severity. Recent developments have shed light on the pathophysiology of RA in smokers, including oxidative stress, inflammation, autoantibody formation and epigenetic changes. The association of smoking and the development of RA have been demonstrated through epidemiologic studies, as well as through in vivo and animal models of RA. With increased use of biological agents in addition to standard disease-modifying antirheumatic drugs (DMARDs), there has been interest in how smoking affects drug response in RA treatment. Recent evidence suggests the response and drug survival in people treated with anti-tumour necrosis factor (anti-TNF) therapy is poorer in heavy smokers, and possible immunological mechanisms for this effect are presented in the current paper.
Highlights
Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by persistent synovitis and the production of auto-antibodies against various factors, including rheumatoid factor (RF) and cyclic citrullinated peptide (CCP) [1,2]
We describe the known immunobiologic effects of cigarette smoking, the epidemiologic studies implicating smoking with increased risk of RA, the effect of smoking on synovial fibroblasts and the impact of smoking on the response to anti-tumour necrosis factor therapy
The disease risk of RF-positive RA associated with the shared epitope (SE) of human leukocyte antigen (HLA)-DR is strongly influenced by the presence of an environmental factor in the population at risk
Summary
Rheumatoid arthritis (RA) is a systemic inflammatory disease characterized by persistent synovitis and the production of auto-antibodies against various factors, including rheumatoid factor (RF) and cyclic citrullinated peptide (CCP) [1,2]. It is well established that genetic factors, such as human leukocyte antigen (HLA), and environmental factors, such as infection, ultraviolet, radiation and smoking, can affect the development of various autoimmune diseases [1,2,3]. Among these factors, cigarette smoking significantly increases the risk of various types of cancer, cardiopulmonary diseases and infections, and autoimmune diseases, such as systemic lupus erythematosus and RA [4,5,6,7,8]. The exact pathogenic effect of smoking on RA still remains uncertain, several mechanisms have been proposed to better understand how cigarette smoking plays a role in various autoimmune diseases [3,4,5,6,7,8], and citrullination has been reported to be an important factor for the development of RA in the anti-citrullinated protein antibody (ACPA)-positive subset
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