Fig. 3

Expression of the microglial CX₃CR1 is decreased in Cx₃cl1^105Δ mice. a, c Flow cytometry on isolated brain mononuclear cells revealed no alteration in the total number of resident microglia in Non-Tg, Cx₃cl1^−/−, or Cx₃cl1^105Δ mice (Cd11b⁺/CD45^low). b, d Overall decreased CX₃CR1 expression in the CD11b⁺CD45^low (microglial population) in Cx₃cl1^105Δ mice compared to Non-Tg and Cx₃cl1^−/− mice (mean + SEM; one-way ANOVA followed by Tukey’s post hoc test: *p < 0.05, **p < 0.01; n = 3 mice per group). e Working model of microglial-neuronal fractalkine signaling axis. Note that the neuronal-derived CX₃CL1 either as full length (in case of Non-Tg mice), as complete knockout (in Cx₃cl1^−/− mice), or as the only soluble form with chemokine domain (Cx₃cl1^105Δ mice) differentially regulates the expression of microglial CX₃CR1 (which is a seven transmembrane G protein-coupled receptor) on the cell surface. This in turn may lead to over-activation of microglia in (Cx₃cl1^105Δ mice) and enhanced neuroinflammation and exacerbation of tau pathology in chemical (LPS) or genetic (hTau) model of tauopathy