NDLI: Retinoic acid attenuates rheumatoid inflammation in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Jennifer Kwok, Seung-Ki Kim, Ho-Youn Park, Sung-Hwan Cho, Mi-La Lee, Dong-Gun Park, Mi-Kyung Park, Eun-Mi Oh, Hye-Jwa
Description	Author Affiliation: Kwok SK ( Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea.)
Abstract	Retinoic acid is the active vitamin A derivative and is well-known to have diverse immunomodulatory actions. In this study, we investigated the impact of all-trans retinoic acid (ATRA), a biologic key metabolite of vitamin A, on the development of arthritis and the pathophysiologic mechanisms by which ATRA might have antiarthritic effects in animal model of rheumatoid arthritis (RA; collagen-induced arthritis [CIA] in DBA/1J mice). We showed that treatment with ATRA markedly suppressed the clinical and histologic signs of arthritis in the CIA mice. It reduced the expression of IL-17 in the arthritic joints. Interestingly, Foxp3(+) regulatory T cells were markedly increased and IL-17-producing CD4(+) T cells (Th17 cells) were decreased in the spleens of ATRA-treated mice. In vitro treatment with ATRA induced the expression of Foxp3 and repressed the IL-17 expression in the CD4(+) T cells in mice. ATRA suppressed the production of total IgG and IgG2a in splenocytes that were stimulated by LPS. It also reduced serum levels of total IgG and IgG2 anti-collagen Abs and germinal center formation in CIA mice. In addition, the ATRA-treated mice showed decreased osteoclast formation in arthritic joints. Moreover, ATRA downregulated the expression of receptor activator of NF-κB ligand, the leading player of osteoclastogenesis, in the CD4(+) T cells and fibroblast-like synoviocytes from patients with RA. Furthermore, ATRA prevented both human monocytes and mice bone marrow-derived monocytes/macrophage cells from differentiating into osteoclasts. These data suggest ATRA might be an effective treatment modality for RA patients.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Arthritis, Rheumatoid Drug Therapy Immunology Inflammation Mediators Therapeutic Use Tretinoin Animals Pathology Collagen Type Ii Toxicity Disease Models, Animal Immunity, Humoral Drug Effects Inflammation Administration & Dosage Mice Mice, Inbred Dba Osteoclasts Th17 Cells Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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