CD4+CD25bright regulatory T cells actively regulate inflammation in the joints of patients with the remitting form of juvenile idiopathic arthritis

J Immunol. 2004 May 15;172(10):6435-43. doi: 10.4049/jimmunol.172.10.6435.

Abstract

This study investigates the role of CD4(+)CD25(+) regulatory T cells during the clinical course of juvenile idiopathic arthritis (JIA). Persistent oligoarticular JIA (pers-OA JIA) is a subtype of JIA with a relatively benign, self-remitting course while extended oligoarticular JIA (ext-OA JIA) is a subtype with a much less favorable prognosis. Our data show that patients with pers-OA JIA display a significantly higher frequency of CD4(+)CD25(bright) T cells with concomitant higher levels of mRNA FoxP3 in the peripheral blood than ext-OA JIA patients. Furthermore, while numbers of synovial fluid (SF) CD4(+)CD25(bright) T cells were equal in both patient groups, pers-OA JIA patients displayed a higher frequency of CD4(+)CD25(int) T cells and therefore of CD4(+)CD25(total) in the SF than ext-OA JIA patients. Analysis of FoxP3 mRNA levels revealed a high expression in SF CD4(+)CD25(bright) T cells of both patient groups and also significant expression of FoxP3 mRNA in the CD4(+)CD25(int) T cell population. The CD4(+)CD25(bright) cells of both patient groups and the CD4(+)CD25(int) cells of pers-OA JIA patients were able to suppress responses of CD25(neg) cells in vitro. A markedly higher expression of CTLA-4, glucocorticoid-induced TNFR, and HLA-DR on SF CD4(+)CD25(bright) T regulatory (Treg) cells compared with their peripheral counterparts suggests that the CD4(+)CD25(+) Treg cells may undergo maturation in the joint. In correlation with this mature phenotype, the SF CD4(+)CD25(bright) T cells showed an increased regulatory capacity in vitro compared with peripheral blood CD4(+)CD25(bright) T cells. These data suggest that CD4(+)CD25(bright) Treg cells play a role in determining the patient's fate toward either a favorable or unfavorable clinical course of disease.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Arthritis, Juvenile / blood
  • Arthritis, Juvenile / immunology*
  • Arthritis, Juvenile / pathology*
  • Biomarkers / blood
  • CD4-Positive T-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / pathology
  • Cartilage, Articular / immunology*
  • Cartilage, Articular / pathology*
  • Cell Differentiation / immunology
  • Child
  • Child, Preschool
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / blood
  • Female
  • Forkhead Transcription Factors
  • Humans
  • Interferon-gamma / antagonists & inhibitors
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / genetics
  • Interleukin-10 / biosynthesis
  • Interleukin-10 / genetics
  • Interleukin-2 / pharmacology
  • Leukocytes, Mononuclear / immunology
  • Leukocytes, Mononuclear / pathology
  • Lymphocyte Count
  • Male
  • RNA, Messenger / antagonists & inhibitors
  • RNA, Messenger / biosynthesis
  • Receptors, Interleukin-2 / biosynthesis*
  • Receptors, Interleukin-2 / blood
  • Receptors, Interleukin-2 / metabolism
  • Remission, Spontaneous
  • Synovial Fluid / cytology
  • Synovial Fluid / immunology
  • Synovial Fluid / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • T-Lymphocytes, Regulatory / pathology
  • Transforming Growth Factor beta / biosynthesis
  • Transforming Growth Factor beta / genetics
  • Up-Regulation / immunology

Substances

  • Biomarkers
  • DNA-Binding Proteins
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Interleukin-2
  • RNA, Messenger
  • Receptors, Interleukin-2
  • Transforming Growth Factor beta
  • Interleukin-10
  • Interferon-gamma