The inflammatory disease–associated variants in IL12B and IL23R are not associated with rheumatoid arthritis

Abstract

There is increasing evidence that common genetic variants can contribute to general immune dysregulation and susceptibility to noninfectious inflammatory diseases. The cytotoxic T-lymphocyte-associated protein 4 (CTLA4) has been associated with Graves disease, type 1 diabetes (T1D), Addison’s disease, celiac disease and rheumatoid arthritis (RA) with odds ratios (ORs) ranging from 1.1 to 1.5 (1). In addition, a missense SNP, rs2476601, in the intracellular tyrosine phosphatase, PTPN22, has been found to be a risk factor (OR = 1.4–2.0) for a number of autoimmune diseases including RA, T1D, autoimmune thyroid disease and systemic lupus erythematosis (SLE) (1) while variants in the third intron of the transcription factor, STAT4, have been associated with risk to both RA and SLE (OR = 1.2–1.8) (2). Finally, the recent plethora of whole genome association (WGA) publications suggests common variants in other genes such as PTPN2 and IL2RA may contribute to risk of multiple noninfectious inflammatory diseases (3,4).