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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.

Pubmed ID: 17182110


  • Carter LL
  • Leach MW
  • Azoitei ML
  • Cui J
  • Pelker JW
  • Jussif J
  • Benoit S
  • Ireland G
  • Luxenberg D
  • Askew GR
  • Milarski KL
  • Groves C
  • Brown T
  • Carito BA
  • Percival K
  • Carreno BM
  • Collins M
  • Marusic S


Journal of neuroimmunology

Publication Data

January 8, 2007

Associated Grants


Mesh Terms

  • Animals
  • Antigens, CD274
  • Antigens, CD80
  • Antigens, Differentiation
  • Encephalomyelitis, Autoimmune, Experimental
  • Glycoproteins
  • Humans
  • Interferon-gamma
  • Interleukin-17
  • Interleukin-6
  • Lymph Nodes
  • Lymphocyte Activation
  • Membrane Glycoproteins
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Myelin-Oligodendrocyte Glycoprotein
  • Peptide Fragments
  • Peptides
  • Programmed Cell Death 1 Ligand 2 Protein
  • Programmed Cell Death 1 Receptor
  • Severity of Illness Index
  • T-Lymphocytes
  • Tumor Necrosis Factor-alpha