KMID : 1144820180240040305
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´ëÇÑÀÇ»ý¸í°úÇÐȸÁö 2018 Volume.24 No. 4 p.305 ~ p.310
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Crosstalk Signaling between IFN-¥ã and TGF-¥â in Microglia Restores the Defective ¥â-amyloid Clearance Pathway in Aging Mice with Alzheimer's Disease
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Choi Go-Eun
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Abstract
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Microglia are emerging as critical regulators of innate immune responses in AD and other neurodegenerative disorders, highlighting the importance of understanding their molecular and cellular mechanisms. We attempted to determine the role of crosstalk signaling between IFN-¥ã and TGF-¥â in A¥â clearance by microglia cells. We used in vitro and in vivo mouse models that recapitulated acute and chronic aspects of microglial responses to A¥â peptides. We showed that crosstalk signaling between TGF-¥â and Smad2 was an important mediator of neuro-inflammation. These findings suggest that microglial TGF-¥â activity enhances the pathological progression to AD. As TGF-¥â displays broad regulatory effects on beneficial microglial functions, the activation of inflammatory crosstalk signaling between TGF-¥â and Smad2 may be a promising strategy to restore microglial functions, halt the progression of A¥â-driven pathology, and prevent AD development.
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KEYWORD
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Alzheimer's disease, Microglia, IFN-¥ã, TGF-¥â, APPswe transgenic mice
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