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J Neuroimmunol. 2007 Jan;182(1-2):124-34. Epub 2006 Dec 19.

PD-1/PD-L1, but not PD-1/PD-L2, interactions regulate the severity of experimental autoimmune encephalomyelitis.

Author information

1
Inflammation, Wyeth Research, 200 CambridgePark Dr., Cambridge, MA 02140, United States. lcarter@wyeth.com

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.

PMID:
17182110
DOI:
10.1016/j.jneuroim.2006.10.006
[Indexed for MEDLINE]

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