Expression of CX3CR1 and CCR2 in brain lesions of mice with EAE.

(A–C) Low-magnification epifluorescence images of naive Ccr2^RFP/+Cx3cr1^GFP/+ (A), diseased Ccr2^RFP/+Cx3cr1^GFP/+ (B), and Ccr2^RFP/RFPCx3cr1^GFP/+ (C) brains show the extent of inflammation and anatomical location of the lesions. Higher magnification views of the boxed areas are shown in panels D–F. Confocal image of healthy perivascular (D) tissue shows GFP⁺ microglia (asterisks), small round RFP⁺ cells (arrowhead), and double-positive cells (circles). (E) Parenchymal lesion in a Ccr2^RFP/+Cx3cr1^GFP/+mouse and (F) a perivascular lesion from a Ccr2^RFP/RFPCx3cr1^GFP/+ mouse at peak EAE disease. Dashed line in (F) indicates the approximate perivascular boundary. Within EAE lesions, note RFP/GFP double-positive cells (circles), GFP⁺ activated microglia (E, F; asterisks), large elongated RFP⁺ cells (E, F; arrows), and small round RFP⁺ cells (E, F; arrowheads). Small RFP⁺ cells were CD3⁺ (not shown). The particularly elongated RFP⁺ cells in the Ccr2^RFP/+Cx3cr1^GFP/+ lesion (E) were much less abundant in the Ccr2^RFP/RFPCx3cr1^GFP/+ lesion (F).