Dysregulation in Retinal Para-Inflammation and Age-Related Retinal Degeneration in CCL2 or CCR2 Deficient Mice 英文参考文献.docVIP

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Dysregulation in Retinal Para-Inflammation and Age-Related Retinal Degeneration in CCL2 or CCR2 Deficient Mice 英文参考文献.doc

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Dysregulation in Retinal Para-Inflammation and Age-Related Retinal Degeneration in CCL2 or CCR2 Deficient Mice 英文参考文献

DysregulationinRetinalPara-InflammationandAge- RelatedRetinalDegenerationinCCL2orCCR2Deficient Mice MeiChen1,JohnV.Forrester2,HepingXu1* 1Centre for Vision andVascularScience, Queen’sUniversity Belfast, Belfast,United Kingdom, 2Immunologyand Infection, University ofAberdeen, Aberdeen, United Kingdom Abstract Wehaveshownpreviouslythatapara-inflammatoryresponseexistsattheretinal/choroidalinterfaceintheagingeye;and thisresponseplaysanimportantroleinmaintainingretinalhomeostasisunderchronicstressconditions.Wehypothesized thatdysregulationof thepara-inflammatory responsemay resultin anovert pro-inflammatory responseinducingretinal degeneration.Inthisstudy,weexaminedthishypothesisinmicedeficientinchemokineCCL2oritscognatereceptorCCR2. CCL2-orCCR2-deficientmicedevelopedretinaldegenerativechangeswithage,characterizedasretinalpigmentepithelial (RPE) cell and photoreceptor cell death. Retinal cell death was associated with significantly more subretinal microglial accumulation and increased complement activation. In addition, monocytes from CCL2- or CCR2-deficient mice had reducedcapacityforphagocytosisandchemotaxis,expressedlessIL-10butmoreiNOS,IL-12andTNF-awhencomparedto monocytes from WT mice. Complement activation at the site of RPE cell death resulted in C3b/C3d but not C5b-9 deposition, indicating only partial activation of the complement pathway. Our results suggest that altered monocyte functions may convert the protective para-inflammatory response into an overtly harmful inflammation at the retina/ choroidalinterfaceinCCL2-orCCR2-deficientmice,leadingtoRPEandphotoreceptordegeneration.Thesedatasupporta conceptwherebyaprotectivepara-inflammatoryresponsereliesuponanormallyfunctioninginnateimmunesystem.Ifthe innateimmunesystemisdeficientchronicstressmaytipthebalancetowardsanovertinflammatoryresponsecausingcell/ tissuedamage. Citation: Chen M, Forrester JV, Xu H (2011) Dysregulation in Retinal Para-Inflammation and Age-Related Retinal Degeneration in CCL2 or CCR2 Defic