Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3065854 | Journal of Neuroimmunology | 2007 | 11 Pages |
Abstract
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-γ, 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.
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Authors
Laura L. Carter, Michael W. Leach, Mihai L. Azoitei, Junqing Cui, Jeffrey W. Pelker, Jason Jussif, Steve Benoit, Gretchen Ireland, Deborah Luxenberg, G. Roger Askew, Kim L. Milarski, Christopher Groves, Tom Brown, Brenda A. Carito, Karen Percival,