Cytosolic phospholipase A2α gene silencing in monocytes alters development of Th1 responses and reduces autoimmune arthritis.

Monocytes play a key role in both the systemic and local progression of rheumatoid arthritis (RA) by producing molecules that participate to the inflammatory and catabolic events of disease pathogenesis (1). Recently, the spleen has been shown to contribute to the regulation of inflammation through monocytes that are able to exit and rapidly deploy to inflammatory sites (2). These observations uncover a role for splenic monocytes as a resource exploited by the body to regulate inflammation. Thus, the engineering of vectors tailored to selectively target both tissue resident and circulating monocytes is a promising research track for addressing the role of specific genes in RA pathogenicity. Several lines of evidence imply cytosolic phospholipase A2α (cPLA2α) as a critical enzyme in inflammatory disorders including RA.