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Title: CCR2 and CX3CR1 in monocyte trafficking in experimental autoimmune uveoretinitis
Author: Dagkalis, Athanasios
ISNI:       0000 0004 2668 3444
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2008
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We used Experimental Autoimmune Uveoretinitis (EAU) as a model system to investigate the involvement of CCR2 and CX3CR1 in regulating the trafficking and function of monocytes and microglia in an autoimmune context. METHODS: W.T. or CX3CR1GFP/GFP monocytes were adoptively transferred into mice with EAU.  At 48 hours post transfer their phenotype was examined by flow cytometry and monocytes trafficking to the retina was imaged using Scanning Laser Ophthalmoscopy. An anti-CCR2 antibody (MC21) or antagonist (JE(9-76)) was used to examine the effect of CCR2 blockade on W.T. monocytes trafficking.  Infiltration of monocytes into the inflamed retina and activation of retinal microglia were examined by confocal microscopy on retinal flatmounts from W.T. and CX3CR1GFP/GFP mice and immunohistochemistry on cryosections from eyes. RESULTS: CCR2 increased on W.T. monocytes at 48 hours post transfer and at 24 hours on CX3CR1GFP/GFP monocytes.  However, blocking CCR2 by either method did not reduce the number of W.T. monocytes rolling along retinal vessels and infiltrating the retina.  Lack of CX3CR1 did not alter microglial activation but infiltrating monocytes lacking the receptor could not migrate through the retina and clustered around vessels. CONCLSIONS: CCR2 may  not always be needed for recruitment into an inflammatory site.  CX3CR1 has a role in neuroprotection in the retina by enhancing the migratory ability and distribution of infiltrating monocytes within inflamed tissue.  This work stresses the importance for careful dissection of the chemokine receptors’ mechanism of action before therapeutic possibilities are explored.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: Chemokines ; Cell receptors ; Inflammation