期刊
NEUROBIOLOGY OF DISEASE
卷 56, 期 -, 页码 59-65出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2013.04.009
关键词
Th1 cells; Th17 cells; Apolipoprotein E; Mimetic peptide; Experimental autoimmune encephalomyelitis
资金
- National Natural Science Foundation of China [81260188]
- Guangxi Higher Education research project [201204LX050]
- Guangxi Natural Science Foundation [0991009, 2012GXNSFAA053082]
Apolipoprotein E (apoE) has been detected to possess anti-inflammatory properties that can contribute to protection against experimental autoimmune encephalomyelitis (EAE). However, its impact on Th1 and Th17 responses in EAE is unclear. In this study, we induced EAE in apoE-/- mice and wild-type mice. We observed that the absence of apoE resulted in the increased proportion of Th1 and Th17 cells in the spleens and brains, as well as up-regulated expressions of proinflammatory cytokines (IL-17, IFN-gamma, TNF-alpha, IL-12, IL-1 beta and IL-6) and transcription factors (ROR gamma t and T-bet) in the CNS. ApoE-/- mice also showed the increased release of proinflammatory cytokines by macrophages in vitro. In addition, we used a mimetic peptide of apoE, which mimic the functions of apoE except for lipid transport. ApoE mimetic peptide could reverse the above negative effect in EAE. Thus, apoE can modulate Th1 and Th17 responses, likely through its inhibitory effect on the secretion of cytokines by macrophages. Our result also suggests that apoE mimetic peptide might be developed into a therapeutic agent for multiple sclerosis. (c) 2013 Elsevier Inc. All rights reserved.
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