RA is a complex and poorly understood disease. However, the characteristic presence of antibodies to citrullinated proteins (anti-CCP) suggests that there are pathogenic mechanisms unique to RA. Recent studies suggest a link between smoking, HLA-DRBSE, anti-CCP and RA. Smoking has long been linked to RA and worsens articular disease as well as<unk> . Exposure to cigarette smoke leads to the activation of PADI enzymes that deaminate arginine to citrulline, producing autoantigens like citrullinated collagen and fibrinogen. Autoantigenic peptides containing citrulline residues are preferentially bound by HLA-DRB SE proteins and are presented to T cells, which interact with CCP-specific B cells found at sites containing autoantigen and produce inflammatory cytokines and autoantibodies, which accelerate disease. Bacterial or viral infections of the respiratory tract may also exacerbate pulmonary inflammation and<unk> .
Rheumatoid lung disease
Mineral dust airway disease
Alcoholic lung disease
Allergic bronchopulmonary aspergillosis
Idiopathic pulmonary fibrosis
Bronchiectasis
Alveolar lung disease
Plastic bronchitis