TGF-beta-treated antigen presenting cells suppress collagen-induced arthritis through the promotion of Th2 responses.
10.3858/emm.2010.42.3.019
- Author:
Sundo JUNG
1
;
Yoon Kyung PARK
;
Hyunji LEE
;
Jung Hoon SHIN
;
Gap Ryol LEE
;
Se Ho PARK
Author Information
1. School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea. sehopark@korea.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
antigen-presenting cells;
arthritis, experimental;
autoimmune diseases;
immune tolerance;
Th1 cells;
Th2 cells
- MeSH:
Animals;
Antigen-Presenting Cells/*drug effects/*immunology;
Arthritis, Experimental/*immunology;
Chickens;
Collagen Type II/immunology;
Immune Tolerance/drug effects;
Mice;
Mice, Inbred BALB C;
Ovalbumin/immunology;
Th1 Cells/drug effects/immunology;
Th2 Cells/*drug effects/*immunology;
Transforming Growth Factor beta2/*pharmacology
- From:Experimental & Molecular Medicine
2010;42(3):187-194
- CountryRepublic of Korea
- Language:English
-
Abstract:
Collagen-induced arthritis (CIA) is mediated by self-reactive CD4+ T cells that produce inflammatory cytokines. TGF-beta2-treated tolerogenic antigen-presenting cells (Tol-APCs) are known to induce tolerance in various autoimmune diseases. In this study, we investigated whether collagen-specific Tol-APCs could induce suppression of CIA. We observed that Tol-APCs could suppress the development and severity of CIA and delay the onset of CIA. Treatment of Tol-APCs reduced the number of IFN-gamma- and IL-17-producing CD4+ T cells and increased IL-4- and IL-5-producing CD4+ T cells upon collagen antigen stimulation in vitro. The suppression of CIA conferred by Tol-APCs correlated with their ability to selectively induce IL-10 production. We also observed that treatment of Tol-APCs inhibited not only cellular immune responses but also humoral immune responses in the process of CIA. Our results suggest that in vitro-generated Tol-APCs have potential therapeutic value for the treatment of rheumatoid arthritis as well as other autoimmune diseases.
