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,
Beatriz M Carreno,
Mary Collins,
Suzana Marusic
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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-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.
Journal of Neuroimmunology 02/2007; 182(1-2):124-34. · 2.96 Impact Factor
