Increased Indoleamine 2,3-Dioxygenase Expressing CD11c+ CD11b+ Dendritic cells in Oral Tolerance to Type II Collagen.
10.4078/jkra.2008.15.4.306
- Author:
Young Joo KIM
1
;
Ho Youn KIM
;
Min Jung PARK
;
So Youn MIN
;
Hyun Sil PARK
;
Mi La CHO
Author Information
1. The Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, Korea. ho0919@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
CD11c+CD11b+ dendritic cells;
Indoleamine 2,3-dioxygenase (IDO);
Oral tolerance;
Regulatory T cell;
Autoimmune arthritis
- MeSH:
Mice;
Animals
- From:The Journal of the Korean Rheumatism Association
2008;15(4):306-316
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: Indoleamine 2, 3-dioxygenase (IDO), an immuno suppression enzyme, is one of the initial and rate-limiting enzymes involved in the catabolism of the essential amino acid tryptophan. IDO inhibits T cell proliferation, induces T cell apoptosis, and plays a fundamental role in autoimmunity and allergy. We investigated which subtype of dendritic cells (DCs) is involved in IDO expression and the generation of regulatory T cells during the induction of oral tolerance in type II collagen-induced arthritis (CIA). METHODS: Type II Collagen was fed to DBA/1J mice before immunization. Changes in DC subtypes and induction of regulatory T cell in orally tolerized CIA mice were analyzed. Whether the effect of DC subtype was modulated by the IDO expression, was determined by flow cytometry (FACs) and confocal microscopy. RESULTS: IDO expression of CD11c+ DCs was higher in orally tolerized CIA mice than in non-tolerized CIA mice. CD11b+ DCs of the CD11c +DCs, subtype was higher in the induction of in IDO expression. Our data suggest that these IDO expressing DCs of oral tolerized mice suppressed type II collagen-specific T cell proliferation and favored the differentiation of naive CD4+ T cells into regulatory T cells. Especially, CD11c+CD11b+ DCs expressed IDO, which is known to be associated with regulatory T cell induction. CONCLUSION: We observed that oral tolerance induced the increase in IDO-expressing CD11c+CD11b+ DCs, which appeared to induce regulatory T cells. IDO-expressing CD11c+CD11b+ DCs are involved in oral tolerance, which may provide a new therapeutic approach for the treatment of rheumatoid arthritis.
