Interleukin 10 regulates cell surface and soluble LIR-2 (CD85d) expression on dendritic cells resulting in T cell hyporesponsiveness in vitro

Eur J Immunol. 2004 Jan;34(1):74-80. doi: 10.1002/eji.200324550.

Abstract

Dendritic cells (DC) are unique in their ability to stimulate naive T cells to proliferate and to differentiate into effector T cells. DC, however, can also inhibit T cell activation and play a role in central and peripheral tolerance. IL-10 has been shown to render DC tolerogenic by unknown mechanisms. Using a combined monoclonal antibody/retroviral expression cloning approach, we show here that the inhibitory receptor LIR-2 (leukocyte immunoglobulin-like receptor-2, CD85d) is specifically up-regulated by IL-10 on maturing human DC. LPS-stimulated, LIR-2-transfected DC inhibited the proliferation of T cells in autologous, as well as allogeneic culture systems in vitro. In addition, overexpression of LIR-2 on resting T cells, which lack LIR-2 expression, inhibited T cell proliferation induced by TCR activation. A novel soluble form of LIR-2 was detected in culture supernatants of maturing DC. IL-10 treatment of DC potently inhibited the production of soluble LIR-2. Recombinant soluble LIR-2 was able to completely restore the proliferation of T cells activated with LPS-plus IL-10-treated DC. Thus, IL-10 renders DC hypostimulatory by up-regulating cell surface LIR-2 and by inhibiting soluble LIR-2 in vitro.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Division / physiology
  • Dendritic Cells / immunology*
  • Dendritic Cells / metabolism
  • Humans
  • Interleukin-10 / metabolism*
  • Lipopolysaccharides / metabolism
  • Membrane Glycoproteins
  • Mice
  • Receptors, Immunologic / biosynthesis
  • Receptors, Immunologic / genetics*
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / physiology
  • Transfection

Substances

  • LILRB2 protein, human
  • Lipopolysaccharides
  • Membrane Glycoproteins
  • Receptors, Immunologic
  • Interleukin-10