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- Publisher
- Oxford University Press
- Copyright
- The Japanese Society for Immunology
- ISSN
- 0953-8178
- eISSN
- 1460-2377
- DOI
- 10.1093/intimm/dxh029
- Publisher site
- See Article on Publisher Site
Abstract
CD25+CD4+ regulatory T cells inhibit the activation of autoreactive T cells in vitro and in vivo, and suppress organ‐specific autoimmune diseases. The mechanism of CD25+CD4+ T cells in the regulation of experimental autoimmune encephalomyelitis (EAE) is poorly understood. To assess the role of CD25+CD4+ T cells in EAE, SJL mice were immunized with myelin proteolipid protein (PLP)139–151 to develop EAE and were treated with anti‐CD25 mAb. Treatment with anti‐CD25 antibody following immunization resulted in a significant enhancement of EAE disease severity and mortality. There was increased inflammation in the central nervous system (CNS) of anti‐CD25 mAb‐treated mice. Anti‐CD25 antibody treatment caused a decrease in the percentage of CD25+CD4+ T cells in blood, peripheral lymph node (LN) and spleen associated with increased production of IFN‐γ and a decrease in IL‐10 production by LN cells stimulated with PLP130–151 in vitro. In addition, transfer of CD25+CD4+ regulatory T cells from naive SJL mice decreased the severity of active EAE. In vitro, anti‐CD3‐stimulated CD25+CD4+ T cells from naive SJL mice secreted IL‐10 and IL‐10 soluble receptor (sR) partially reversed the in vitro suppressive activity of CD25+CD4+ T cells. CD25+CD4+ T cells from IL‐10‐deficient mice were unable to suppress active EAE. These findings demonstrate that CD25+CD4+ T cells suppress pathogenic autoreactive T cells in actively induced EAE and suggest they may play an important natural regulatory function in controlling CNS autoimmune disease through a mechanism that involves IL‐10.
Journal
International Immunology – Oxford University Press
Published: Feb 1, 2004