PTPRC and infection: Using a validated gating strategy,[31] resident microglia (Ly6G−, SSCAlo, NK1.1−, CD3e−, B220−, CD45low–int, CX3CR1+, Ly6Clo), brain‐infiltrating MCs (defined as Ly6G−, SSCAlo, NK1.1−, CD3e−, B220−, CD45hi, CX3CR1low, Ly6Chi) and BM monocytes (defined as Ly6G−, SSCAlo, NK1.1−, CD3e−, B220−, CD11clo, MHC‐IIlo, CD11b+, Ly6Chi/lo, CX3CR1hi/lo) clustered into 8 distinct metabolic states which varied in proportion across timepoints and were distinctly grouped by organ and lineage/differentiation status (Figure 2C–H), demonstrating a significant metabolic adaptation over the course of infection.