PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis
pmid: 17182110
PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis
Interactions between PD-1 and its two differentially expressed ligands, PD-L1 and PD-L2, attenuate T cell activation and effector function. To determine the role of these molecules in autoimmune disease of the CNS, PD-1-/-, PD-L1-/- and PD-L2-/- mice were generated and immunized to induce experimental autoimmune encephalomyelitis (EAE). PD-1-/- and PD-L1-/- mice developed more severe EAE than wild type and PD-L2-/- mice. Consistent with this, PD-1-/- and PD-L1-/- cells produced elevated levels of the pro-inflammatory cytokines IFN-gamma, TNF, IL-6 and IL-17. These results demonstrate that interactions between PD-1/PD-L1, but not PD-1/PDL-2, are crucial in attenuating T cell responses in EAE.
Mice, Knockout, Encephalomyelitis, Autoimmune, Experimental, Membrane Glycoproteins, Interleukin-6, Interleukin-17, Mice, Transgenic, Lymphocyte Activation, Programmed Cell Death 1 Ligand 2 Protein, Antigens, Differentiation, B7-H1 Antigen, Peptide Fragments, Interferon-gamma, Mice, B7-1 Antigen, Animals, Humans, Myelin-Oligodendrocyte Glycoprotein, Lymph Nodes, Peptides, Glycoproteins
Mice, Knockout, Encephalomyelitis, Autoimmune, Experimental, Membrane Glycoproteins, Interleukin-6, Interleukin-17, Mice, Transgenic, Lymphocyte Activation, Programmed Cell Death 1 Ligand 2 Protein, Antigens, Differentiation, B7-H1 Antigen, Peptide Fragments, Interferon-gamma, Mice, B7-1 Antigen, Animals, Humans, Myelin-Oligodendrocyte Glycoprotein, Lymph Nodes, Peptides, Glycoproteins
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