Non-classical pathways of cell-mediated allograft rejection: new challenges for tolerance induction?

Am J Transplant. 2003 Feb;3(2):101-6. doi: 10.1034/j.1600-6143.2002.00026.x.

Abstract

Allograft rejection results from separate pathways primarily controlled by CD4+ T cells. Refinement of transplantation models together with investigations on rejection occurring despite co-stimulation blockade revealed unexpected pathways involving CD8+ T cells, NK cells and Th2 cytokines. In this minireview, we discuss these non-classical pathways of allograft rejection and their relevance for the induction of tolerance in the clinics.

Publication types

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

MeSH terms

  • Animals
  • Antigens / immunology
  • Antigens, Surface
  • CD8-Positive T-Lymphocytes / immunology
  • Disease Models, Animal
  • Fas Ligand Protein
  • Graft Rejection / immunology*
  • Heart Transplantation / immunology
  • Humans
  • Immunity, Cellular / immunology*
  • Interleukin-2 / immunology
  • Kidney Transplantation / immunology
  • Lectins, C-Type
  • Membrane Glycoproteins / immunology
  • Mice
  • NK Cell Lectin-Like Receptor Subfamily B
  • Proteins / immunology
  • Skin Transplantation / immunology
  • Th2 Cells / immunology
  • Transplantation Tolerance / immunology*

Substances

  • Antigens
  • Antigens, Surface
  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Interleukin-2
  • KLRB1 protein, human
  • Lectins, C-Type
  • Membrane Glycoproteins
  • NK Cell Lectin-Like Receptor Subfamily B
  • Proteins