Since signal transducer and activator of transcription 4 (STAT4) is considered as a significant transcription factor for generation and differentiation of Th1 cells during vascular dysfunction and atherosclerosis, suppressing STAT4 could represent novel immunomodulatory therapies against atherosclerosis.
Although the proinflammatory role of STAT4 in atherosclerosis and diet-induced insulin resistance (IR) was recently established, the impact of STAT4 on atherogenesis in conditions of IR is not known.
To determine whether the PTPN22, STAT4 and TRAF1/C5 gene polymorphisms may be implicated in the development of cardiovascular (CV) events and subclinical atherosclerosis manifested by the presence of endothelial dysfunction or increased carotid intima-media thickness (IMT) in a series of Spanish patients with rheumatoid arthritis (RA).