Enrichment analysis identied overrepresentation of functions related to neuronal development and differentiation, as well as terms and pathways related to cell proliferation, in ischemic microglia compared with eYFP cells of PA ischemic WT mice. Gene set enrichment analysis also identied overrepresentation in microglia of genes involved in the cell division cycle, including GM checkpoint, mitotic spindle assembly, cell cyclerelated targets of EF transcription factors, and genes associated with spermatogenesis. Bars show mean SEM and symbols show individual values per each mouse.We then studied the identity of peripheral eYFP cells inltrating the ischemic brain tissue of WT PA mice by phenotyping DC subsets by ow cytometry.Notably, ischemia induced mRNA expression of chemokines binding those DC receptors at different time points. We isolated microglia, astrocytes, and endothelial cells from control brain tissue and days postischemia to identify which brain cells express these chemokines.To nd out whether microglia contributed to DC inltration to the ischemic brain tissue, we used a pharmacological strategy to deplete microglia.Given that microglial cell viability is CSFR dependent, chronic treatment with the CSFR inhibitor PLX provided in the diet causes strong microglial depletion. Of note, cDC showed a stronger reduction than the other DC subsets after microglia depletion. After weeks we studied the brain of each pair, or we induced brain ischemia in the WT mouse of each pair and studied the brain days later and after ischemia. At steady state, the number of eYFP cells. The representation includes natural clusters found by unsupervised clustering: subclusters PA were upregulated in PA samples, and subcluster mG was upregulated in microglia.Subclusters contained, and genes, respectively.To test this possibility, we blocked CCR by systemic to WT mice. The neurological score and the sizes of the Targetmol’s Valsartan lesion were not different between groups before treatment, as assessed by MRI and behavioral tests Targetmol’s Cyproheptadine hydrochloride hpostischemia, prior to drug administration.Drug treatment did not modify the size of the lesion versus the vehicle days postischemia. Batf mice showed larger infarctions and worse neurological decits than WT mice. The population of microglial cells is heterogeneous and shows phenotypic and functional diversity. Necrotic cell death induced by ischemia generates dangerassociated molecular patterns. ACKR, a scavenger of CXCL, was previously found in microglia in which expression increased under inammatory stimuli. Accordingly, microglia depletion reduced ischemiainduced expression of chemokines in brain and attenuated DC inltration, particularly of cDC.After days of treatment, ischemia was induced, and brain was studied days later using ow cytometry.Bars show group mean SEM and points are values per mouse.We monitored the brain lesion using MRI and assessed the neurological function with a neuroscore. Brain tissue was studied at day using ow cytometry.OXL binds OX on T cells to stimulate clonal expansion of effector and memory T cells. Notably, in the ischemic brain, OXL was expressed by cDC cells and not by other inltrating DC populations or microglia.Moreover, cDC regulate complex innate immune responses that may contribute to their effect on stroke outcome.Phenotypic differences dened and direct ex vivo antigen presentation to myelin basic proteinreactive CD T cells compared.Science.