Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis

Science. 1994 Aug 26;265(5176):1237-40. doi: 10.1126/science.7520605.

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a cell-mediated autoimmune disease that serves as an animal model for multiple sclerosis. Oral administration of myelin basic protein (MBP) suppresses EAE by inducing peripheral tolerance. T cell clones were isolated from the mesenteric lymph nodes of SJL mice that had been orally tolerized to MBP. These clones were CD4+ and were structurally identical to T helper cell type 1 (TH1) encephalitogenic CD4+ clones in T cell receptor usage, major histocompatibility complex restriction, and epitope recognition. However, they produced transforming growth factor-beta with various amounts of interleukin-4 and interleukin-10 and suppressed EAE induced with either MBP or proteolipid protein. Thus, mucosally derived TH2-like clones induced by oral antigen can actively regulate immune responses in vivo and may represent a different subset of T cells.

Publication types

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

MeSH terms

  • Administration, Oral
  • Amino Acid Sequence
  • Animals
  • CD4-Positive T-Lymphocytes / immunology*
  • Clone Cells
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Epitopes / immunology
  • Immune Tolerance*
  • Interleukin-10 / biosynthesis
  • Interleukin-4 / biosynthesis
  • Lymph Nodes / immunology
  • Major Histocompatibility Complex
  • Mesentery / immunology
  • Mice
  • Molecular Sequence Data
  • Myelin Basic Protein / administration & dosage
  • Myelin Basic Protein / immunology*
  • Myelin Proteins / immunology
  • Myelin Proteolipid Protein
  • Receptors, Antigen, T-Cell / immunology
  • Transforming Growth Factor beta / biosynthesis

Substances

  • Epitopes
  • Myelin Basic Protein
  • Myelin Proteins
  • Myelin Proteolipid Protein
  • Receptors, Antigen, T-Cell
  • Transforming Growth Factor beta
  • Interleukin-10
  • Interleukin-4