Lack of adiponectin leads to increased lymphocyte activation and increased disease severity in a mouse model of multiple sclerosis

Laura Piccio, Claudia Cantoni, Jacob G. Henderson, Daniel Hawiger, Michael Ramsbottom, Robert Mikesell, Jiyoon Ryu, Chyi Song Hsieh, Viviana Cremasco, Wesley Haynes, Lily Q. Dong, Lawrence Chan, Daniela Galimberti, Anne H. Cross

Resultado de la investigación: Articlerevisión exhaustiva

73 Citas (Scopus)

Resumen

Multiple sclerosis (MS) is a presumed autoimmune disease directed against central nervous system (CNS) myelin, in which diet and obesity are implicated as risk factors. Immune responses can be influenced by molecules produced by fat cells, called adipokines. Adiponectin is an adipokine with anti-inflammatory effects. We tested the hypothesis that adiponectin has a protective role in the EAE model for MS, that can be induced by immunization with myelin antigens or transfer of myelin-specific T lymphocytes. Adiponectin deficient (ADPKO) mice developed worse EAE with greater CNS inflammation, demyelination, and axon injury. Lymphocytes from myelin-immunized ADPKO mice proliferated more, produced higher amounts of IFN-γ, IL-17, TNF-α, IL-6, and transferred more severe EAE than wild type (WT) lymphocytes. At EAE peak, the spleen and CNS of ADPKO had fewer regulatory T (Treg) cells than WT mice and during EAE recovery, Foxp3, IL-10 and TGF-β expression levels in the CNS were reduced in ADPKO compared with WT mice. Treatment with globular adiponectin in vivo ameliorated EAE, and was associated with an increase in Treg cells. These data indicate that adiponectin is an important regulator of T-cell functions during EAE, suggesting a new avenue of investigation for MS treatment.

Idioma originalEnglish (US)
Páginas (desde-hasta)2089-2100
Número de páginas12
PublicaciónEuropean Journal of Immunology
Volumen43
N.º8
DOI
EstadoPublished - ago. 2013

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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