The role of novel genes in rheumatoid arthritis pathogenesis

Abstract

Rheumatoid arthritis (RA) is a debilitating disease characterized by chronic symmetric polyarthritis involving peripheral small joints. Heterogeneity in RA pathophysiology extends to a molecular level. Understanding the complicated interaction between genetics, environment, and autoimmunity, and their function in pathogenesis, is necessary for getting further insight into the mechanisms and outcomes that manage disease development and progression. Pharmacogenomics emphasizes the relations of numerous genetic signatures with responses to traditional disease-modifying drugs and biologics. More than 100 genetic susceptibility loci have been recognized for RA through studies directed on patients with longstanding RA compared with healthy controls. So the interaction between genes and the environment may determine who is more susceptible to develop RA. This review pays attention to some recently discovered genetic risk loci in RA; ZNF804a, CDK1, YWHAH 14-3-3 η, and IL-17A. Also, their involvement in the etiology, pathogenesis, and outcome of the disease is explained, aiming to provide new insights into the pathogenesis of RA and the possibility to develop novel therapeutic approaches through targeting these genes.