Lack of adiponectin leads to increased lymphocyte activation and increased disease severity in a mouse model of multiple sclerosis.
Lack of adiponectin leads to increased lymphocyte activation and increased disease severity in a mouse model of multiple sclerosis.
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DOI：
10.1002/eji.201242836
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发表时间：
2013-08
影响因子：
5.4
通讯作者：
Cross AH
中科院分区：
文献类型：
--
作者：
Piccio L;Cantoni C;Henderson JG;Hawiger D;Ramsbottom M;Mikesell R;Ryu J;Hsieh CS;Cremasco V;Haynes W;Dong LQ;Chan L;Galimberti D;Cross AH
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 experimental autoimmune encephalomyelitis (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 ADP KO mice proliferated more, produced higher amounts of IFNγ, IL-17, TNFα, IL-6 and transferred more severe EAE than wild type (WT) lymphocytes. At EAE peak, the spleen and CNS of ADPKO had fewer Tregulatory cells (Tregs) than WT mice and during EAE recovery, Foxp3, IL-10 and TGFβ CNS expression levels were reduced in ADPKO compared to WT mice. Treatment with globular adiponectin (gADP) in vivo ameliorated EAE, and was associated with an increase in Tregs. 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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影响因子：
5.5
作者：
Piccio, Laura;Stark, Jennifer L.;Cross, Anne H.
通讯作者：
Cross, Anne H.
影响因子：
2.9
作者：
Kraszula, Lukasz;Jasinska, Anna;Pietruczuk, Miroslawa
通讯作者：
Pietruczuk, Miroslawa
影响因子：
15.9
作者：
Ouedraogo, Raogo;Gong, Yulan;Scalia, Rosario
通讯作者：
Scalia, Rosario
影响因子：
2.2
作者：
Okamoto, Y;Arita, Y;Matsuzawa, Y
通讯作者：
Matsuzawa, Y
DOI：
10.1073/pnas.0403382101
发表时间：
2004-07-13
影响因子：
11.1
作者：
Hug, C;Wang, J;Lodish, HF
通讯作者：
Lodish, HF