期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 43, 期 8, 页码 2089-2100出版社
WILEY-BLACKWELL
DOI: 10.1002/eji.201242836
关键词
Adiponectin; EAE; Immunomodulation; Multiple sclerosis
类别
资金
- Consortium of MS Centers
- National MS Society (NMSS) [PP1645]
- McDonnell Center for Cellular & Molecular Neurobiology, Nutrition and Obesity Research Center (NORC) [P30 DK056341]
- Fondazione Italiana Sclerosi Multipla (FISM) [2009/R/33]
- Barnes-Jewish Foundation
- National Institutes of Health (NIH) [DK080344]
- Manny and Rosalyn Rosenthal-Dr. John L. Trotter Chair
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-, IL-17, TNF-, 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- 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.
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