IFN-γ signaling to astrocytes does not influence brain inflammation.

<p>(<b>A</b>) CD45^hi bone marrow derived inflammatory cells and CD4⁺ T cells in brains (day 16 p.i.) analyzed by flow cytometry following isolation by Percoll gradients. R1 gate = CD45^hi inflammatory cells; R2 gate = CD4⁺ T cells within R1. Representative of 4 separate experiments at days 14 – 16 p.i. (<b>B</b>) IFN-γ and IL-17 secreting MOG-specific CD4⁺ T cells during acute EAE. Brain derived cells enriched by Percoll gradients at day 16 p.i. stimulated with MOG^35–55 peptide for 4 hrs in the presence of GolgiStop. p>0.05 comparing the frequency of MOG-specific CD4⁺ T cells secreting IFN-γ; p<0.05 comparing IL-17 in wt and GFAPγR1Δ mice. CNS cells pooled from 4 – 5 mice per experiment. Data are representative of 3 – 4 separate experiments at days 14 – 16 p.i. (<b>C</b>) Foxp3⁺ regulatory T cells within CD4⁺ T cells enriched from brain at day 16 p.i. CNS cells pooled from 4 – 5 mice per experiment. p<0.05 comparing wt and GFAPγR1Δ mice. Data are representative of 3 separate experiments at days 14 – 16 p.i.