[go: up one dir, main page]

Induction of a regulatory T cell type 1 response reduces the development of atherosclerosis in apolipoprotein E-knockout mice

Circulation. 2003 Sep 9;108(10):1232-7. doi: 10.1161/01.CIR.0000089083.61317.A1. Epub 2003 Aug 11.

Abstract

Background: T helper type 1 (Th1) response plays a permissive role in atherosclerosis. We hypothesized that adoptive transfer of a novel subtype of T lymphocytes called regulatory T cells type 1 (Tr1) would inhibit Th1 responses by inducing a bystander immune suppression and therefore limit the development of atherosclerosis.

Methods and results: Clones of ovalbumin (OVA)-specific Tr1 cells expanded in vitro were administered intraperitoneally (106 cells per mouse) with their cognate antigen (50 microg of OVA subcutaneously in complete Freund's adjuvant [CFA]) to female apolipoprotein E-knockout mice. A group of mice received only (OVA/CFA) immunization without Tr1 cells. Two other control groups received no immunization and were injected with either Tr1 cells or saline. After 9 weeks of treatment, mice injected with (OVA/CFA)+OVA-specific Tr1 cells showed a significant decrease in Th1 responses, as revealed by a decrease in OVA-specific IgG2a serum levels (P<0.0001), a decrease in the production of interferon-gamma (P<0.001), and an increase in interleukin-10 production (P<0.001) by cultured spleen and lymph T cells compared with controls. In addition, cytokine production by concanavalin A-stimulated spleen cells showed a clear switch to a regulatory immune response in mice treated with (OVA/CFA)+Tr1. This was associated with a significant reduction in atherosclerotic lesion size in both the thoracic aorta and aortic sinus of mice treated with (OVA/CFA)+Tr1 compared with controls (P=0.002 to P<0.0001). Plaques of mice injected with (OVA/CFA)+Tr1 showed significantly lower accumulation of macrophages and T cells than plaques of control mice.

Conclusions: Tr1-type regulatory immune response reduces the development of experimental atherosclerosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adoptive Transfer / methods
  • Animals
  • Apolipoproteins E / deficiency*
  • Apolipoproteins E / genetics
  • Arteriosclerosis / immunology
  • Arteriosclerosis / pathology
  • Arteriosclerosis / prevention & control*
  • Bystander Effect / immunology
  • Cells, Cultured
  • Cholesterol / blood
  • Clone Cells
  • Cytokines / metabolism
  • Female
  • Freund's Adjuvant / immunology
  • Immunoglobulin E / blood
  • Immunoglobulin G / blood
  • Immunosuppression Therapy / methods
  • Interferon-gamma / metabolism
  • Interleukin-10 / metabolism
  • Lymph Nodes / cytology
  • Lymph Nodes / immunology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Ovalbumin / immunology
  • Spleen / cytology
  • Spleen / immunology
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology
  • T-Lymphocytes / physiology*
  • T-Lymphocytes / transplantation
  • Th1 Cells / immunology
  • Th1 Cells / physiology

Substances

  • Apolipoproteins E
  • Cytokines
  • Immunoglobulin G
  • Interleukin-10
  • Immunoglobulin E
  • Interferon-gamma
  • Ovalbumin
  • Freund's Adjuvant
  • Cholesterol