We found that TBI leads to an upregulation of type I interferon (IFN) signature genes in macrophages and a controlled upregulation of inflammatory-related genes in the fibroblast and adaptive immune cell populations.
Given our data demonstrating an appreciable expansion of the meningeal macrophage population following injury (Figure 1e), as well as emerging data suggesting instrumental roles for these cells in TBI pathogenesis (Russo et al., 2018; Roth et al., 2014), we decided to focus first on the response of meningeal macrophages to head trauma.
We also noticed that some of the most significantly upregulated genes contributing to the immune-related GO terms were important for the type I IFN response including Ifnar1, Ifi203, Irf2bp2, and Irf5, amongst others (Figure 2d)
we found that aging alone induced upregulation of meningeal genes involved in antibody production by B cells and type I IFN signaling.
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