Fig 2: Inflammatory cells in the injured wt and Ccr2-/- cortex examined by flow cytometry and qRT-PCR.(a) Cells detected with FITC-CD45 in combination with either APC-PDCA-1 (Bst2) or APC-Cd11c (Itgax) in neocortex of wt or Ccr2-/- mice three days after injury. Upper panel left shows gating for Cd11c. The middle and right panels show wt and Ccr2-/- results, respectively, demonstrating reduced number of Cd11c-positive cells in the Ccr2-/- mice. Lower panel shows that PDCA-1 positive cells were reduced in Ccr2-/- brains. (b) Quantitative flow cytometry data from wt and Ccr2-/- mice three days postinjury. Isotype controls showed only trace signals. (c) Temporal expression patterns of six inflammatory-related transcripts (Itgax, H2-Aa, Bst2, Cxcl10, Lyz2 and Hmox1) after injury in wt and Ccr2-/- brains.

Fig 3: Cell sorting and immunodepletion of dendritic cells in neocortex three days after TBI in wt mice analyzed by qRT-PCR.(a) Cd11c-positive cells sorted on magnetic microbeads expressed enhanced H2-Aa and Itgax levels. In contrast, Bst2 was enriched in cells sorted on anti-PDCA-1 microbeads. (b) Cortical levels of inflammatory transcripts in mice injected with control immunoglobulin or with antibodies directed to PDCA-1. Depletion of pDCs was not accompanied by shifts in Itgax or H2-Aa transcript levels whereas a distinct reduction of Bst2 and Cxcl10 occurred.

Fig 4: Inflammatory-related transcripts measured in Ccl3-/- and Ccr2-/- mice with F2 hybrid background three days postinjury. Lyz2 expression was upregulated in homozygous Ccl3 knockouts but downregulated in Ccr2-/- as in the parental strains, as was Bst2. Both Itgax and Cxcl10 levels were less upregulated in the injured F2 Ccr2-/- brains. Gfap expression increased to the same extent in injured wt and F2 hybrid brains.