alexa PD-1 Interaction with PD-L1 but not PD-L2 on B-cells Mediates Protective Effects of Estrogen against EAE
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

PD-1 Interaction with PD-L1 but not PD-L2 on B-cells Mediates Protective Effects of Estrogen against EAE

Sheetal Bodhankar1,2, Danielle Galipeau2, Arthur A Vandenbark1,2,3 and Halina Offner1,2,4*
1 Neuroimmunology Research, Portland VA Medical Center, Portland, OR, USA
2 Department of Neurology, Oregon Health & Science University, Portland, OR, USA
3 Department of Molecular Microbiology & Immunology, Oregon Health & Science University, Portland, OR, USA
4 Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA
Corresponding Author : Dr. Halina Offner
Neuroimmunology Research
R&D-31, Portland Veterans Affairs Medical Center
3710 SW US Veterans Hospital Rd.
Portland, OR 97239, USA
Fax: +1-503-721-7975
E-mail: [email protected]
Received: April 10, 2013; Accepted: April 30, 2013; Published: May 06, 2013
Citation: Bodhankar S, Galipeau D, Vandenbark AA, Offner H (2013) PD-1 Interaction with PD-L1 but not PD-L2 on B-cells Mediates Protective Effects of Estrogen against EAE. J Clin Cell Immunol 4:143. doi:10.4172/2155-9899.1000143
Copyright: © 2013 Bodhankar S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Increased remissions in multiple sclerosis (MS) during late pregnancy may result from high levels of sex steroids such as estrogen and estriol. Estrogen (E2=17β-estradiol) protects against experimental autoimmune encephalomyelitis (EAE), but the cellular basis for E2-induced protection remains unclear. Treatment with relatively low doses of E2 can protect against clinical and histological signs of MOG-35-55 induced EAE through mechanisms involving the PD-1 coinhibitory pathway and B-cells. The current study evaluated the contribution of PD-1 ligands, PD-L1 and PD-L2, on B-cells in E2-mediated protection against EAE in WT, PD-L1-/- and PD-L2-/- mice. Unlike PD-L2- /- mice that were fully protected against EAE after E2 treatment, E2-implanted PD-L1-/- mice were fully susceptible to EAE, with increased numbers of proliferating Th1/Th17 cells in the periphery and severe cellular infiltration and demyelination in the CNS. Moreover, transfer of B-cells from MOG-immunized PD-L1-/- or PD-L2-/- donors into E2- preconditioned B-cell deficient μMT-/- recipient mice revealed significantly reduced E2-mediated protection against EAE in recipients of PD-L1-/- B-cells, but near-complete protection in recipients of PD-L2-/- B-cells. We conclude that PD-1 interaction with PD-L1 but not PD-L2 on B-cells is crucial for E2-mediated protection in EAE and that strategies that enhance PD-1/PD-L1 interactions might potentiate E2 treatment effects in MS.

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