Retinoid, a derivative of
vitamin A, is a general term used to describe compounds that bind to and activate
retinoic acid receptors [RARs (RARα, RARβ, and RARγ)] and/or
retinoid X receptors [RXRs (RXRα, RXRβ, and RXRγ)]. They have been shown to surpress the differentiation of Th1/Th17 cells and induce the development of Th1/regulatory T cells. They also affect the proliferation of B cells as both an inducer and suppressor. Furthermore,
retinoids may induce the maturation of dendritic cells and production of
interleukin-10 from monocytes/macrophages. We recently demonstrated that
retinoids suppressed the production of
reactive oxygen species, the release of
elastase from neutrophils by inhibiting
mitogen-activated protein kinase signals, and both the migration speed and chemotaxis directionality of neutrophils.
Retinoids, such as
all-trans retinoic acid and
tamibarotene, were previously shown to have positive effects on animal models of several
rheumatic diseases, including
arthritis,
myositis, and
vasculitis in vivo. Moreover,
retinoids have been used in a pilot study to effectively treat patients with
lupus nephritis and
systemic sclerosis. We herein reviewed the effects of
retinoids on immune cells, animal models of
rheumatic diseases, and rheumatic patients.