Abstract
Programmed cell death 1 (PD-1) was isolated in 1992 by subtractive-hybridization technique, as a molecule whose expression is enhanced by apoptotic stimuli. Since then we have been analyzing the function of PD-1 in the regulation of immune responses. Generation of PD-1 deficient mice, pathophysiological analyses of autoimmune diseases in PD-1 deficient mice, identification of two ligands, and analyses of downstream events of PD-1 revealed that PD-1 prevents autoimmunity by inhibiting activation of self-reactive lymphocytes. These findings were further applied on human autoimmune diseases and single nucleotide polymorphisms (SNPs) on human PD-1 gene have been reported to link with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and type I diabetes.
MeSH terms
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Animals
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Antigens, CD
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Antigens, Differentiation / genetics
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Antigens, Differentiation / physiology*
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Antigens, Surface / physiology*
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Apoptosis Regulatory Proteins
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Autoimmune Diseases / genetics
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Autoimmune Diseases / immunology*
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B7-1 Antigen / physiology*
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B7-H1 Antigen
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Humans
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Intercellular Signaling Peptides and Proteins
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Membrane Glycoproteins / physiology*
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Mice
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Peptides / physiology*
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Programmed Cell Death 1 Ligand 2 Protein
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Programmed Cell Death 1 Receptor
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Signal Transduction / genetics
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Signal Transduction / immunology*
Substances
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Antigens, CD
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Antigens, Differentiation
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Antigens, Surface
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Apoptosis Regulatory Proteins
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B7-1 Antigen
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B7-H1 Antigen
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CD274 protein, human
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Cd274 protein, mouse
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Intercellular Signaling Peptides and Proteins
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Membrane Glycoproteins
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PDCD1 protein, human
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PDCD1LG2 protein, human
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Pdcd1 protein, mouse
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Pdcd1lg2 protein, mouse
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Peptides
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Programmed Cell Death 1 Ligand 2 Protein
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Programmed Cell Death 1 Receptor