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
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antigens / immunology
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Antigens, Surface
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CD8-Positive T-Lymphocytes / immunology
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Disease Models, Animal
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Fas Ligand Protein
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Graft Rejection / immunology*
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Heart Transplantation / immunology
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Humans
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Immunity, Cellular / immunology*
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Interleukin-2 / immunology
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Kidney Transplantation / immunology
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Lectins, C-Type
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Membrane Glycoproteins / immunology
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Mice
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NK Cell Lectin-Like Receptor Subfamily B
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Proteins / immunology
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Skin Transplantation / immunology
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Th2 Cells / immunology
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Transplantation Tolerance / immunology*
Substances
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Antigens
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Antigens, Surface
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FASLG protein, human
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Fas Ligand Protein
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Fasl protein, mouse
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Interleukin-2
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KLRB1 protein, human
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Lectins, C-Type
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Membrane Glycoproteins
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NK Cell Lectin-Like Receptor Subfamily B
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Proteins