Skip to main content
. 2017 Aug 2;6(8):e006387. doi: 10.1161/JAHA.117.006387

Figure 6.

Figure 6

CCR5 expression by transferred Tregs plays an important role in their protective effect against blood‐brain barrier (BBB) disruption early after stroke. Splenocytes (Sp), wild type (WT) Tregs or CCR5−/− Tregs (2×106) were adoptively transferred into stroke mice 2 hours after 60 minutes of transient middle cerebral artery occlusion (tMCAO). Brain sections were collected 1 day after tMCAO. A through C, Brain sections were stained for endogenous plasma IgG to detect BBB leakage (n=6/group). A, Representative surface plot images of endogenous IgG from sham or tMCAO mice treated with WT or CCR5−/− Treg. B, Quantification of gray value of brain sections in A. C, Quantification of positive IgG‐stained area of brain sections in A. D through G, Brain sections were stained with Gr‐1, a neutrophil marker, CD3, a T‐cell marker, and F4/80, a macrophage marker (n=6/group). D, Representative images showing the infiltration of Gr‐1+ neutrophils into the ischemic brain. E, Quantification of the number of Gr‐1+ neutrophils in the ischemic brain (n=5/group). F, Quantification of the number of CD3+ T cells in the ischemic brain. G, Quantification of the number of F4/80+ macrophages in the ischemic brain. *P≤0.05, **P≤0.01, ***P≤0.001. CCR5 indicates C‐C chemokine receptor type 5; CTX, cortex; IgG, immunoglobulin G; STR, striatum; Treg, regulatory T cell.