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- Title
CD200 increases alternatively activated macrophages through cAMP-response element binding protein - C/EBP-beta signaling.
- Authors
Hayakawa, Kazuhide; Wang, Xiaohua; Lo, Eng H.
- Abstract
The concept of macrophage polarization toward different phenotypes after CNS injury has been increasingly discussed. Here, we propose that CD200 treatment may help shift pro-inflammatory macrophages to an arginase 1 (Arg1)-, transglutaminase 2 ( TGM2)-, and transforming growth factor beta 1 ( TGF-β)-positive phenotype. Rat macrophages were stimulated by interferon γ and lipopolysaccharide ( LPS) to induce pro-inflammatory phenotypes. Treatment with human CD200-Fc up-regulated expression levels of alternatively activated M2-like markers such as Arg1 and TGM2 but suppressed pro-inflammatory M1-like markers such as toll-like receptor 4, interleukin 1 beta (IL-1β), IL-6, and GM- CSF. Concomitantly, CD200-Fc enhanced (CCAAT/enhancer-binding protein) C/ EBP-beta promoter activity, whereas NF-κB activity was suppressed. Treatment with CD200-Fc also up-regulated potentially beneficial TGF-β expression in macrophages. When C/ EBP-beta signaling was suppressed with siRNA, the effect of CD200-Fc on Arg1, TGM2 and TGF-β up-regulation was canceled. Taken together, these data provide proof-of-principle that targeting CD200 signaling may be a novel therapeutic approach to shift macrophages toward M2-like polarization via modulating c AMP-response element binding protein-C/ EBP-beta transcriptional activity.
- Subjects
TUMOR necrosis factors; CREB protein; ARGINASE; TRANSGLUTAMINASES; TRANSFORMING growth factors-beta; LABORATORY rats; INTERFERON alpha; LIPOPOLYSACCHARIDES
- Publication
Journal of Neurochemistry, 2016, Vol 136, Issue 5, p900
- ISSN
0022-3042
- Publication type
Article
- DOI
10.1111/jnc.13492