Fig. 2

CX3CR1^CRE−ER expression modulated by TAM does not alter peripheral immune profile in diabetic CX3CR1^Cre−ER:R26^iDTR mice. A Experimental design for 2-week DTx treatment in diabetic CX3CR1^Cre−ER:R26^iDTR mice. Diabetes was induced via streptozotocin (STZ) in CX3CR1^CreER:R26^iDTR mice 2 weeks after the last TAM injection. At 6–8 weeks of diabetes, mice received 3 daily doses of 25 ng/g DTx, followed by 1 dose of 25 ng/g DTx every 48 h for a total of 2 weeks. Tissues were collected immediately after the 2-week DTx treatment or after a 2-week recovery period. Control diabetic mice were administered PBS instead of DTx. B–G Flow cytometric quantification of CD45^HiCD11b⁺SSC^Hi neutrophils (B), CD45^HiCD11b⁺SSC^Lo macrophages (C), CD45^HiCD11b⁺Ly6C^Lo tissue resident macrophages (D), CD45^HiCD11b⁺Ly6C^Hi inflammatory macrophages (E), CD45^HiCD11b^–CD11c⁺ conventional dendritic cells (F) and CD45^HiCD11b⁺CD11c⁺ myeloid-derived dendritic cells (G). Data show mean ± SD, n = 4–9 mice per group where each dot represents an individual mouse. *P < 0.05, **P < 0.01, ****P < 0.0001 using Student’s t-test, with Welch’s correction