Table 1.

Beneficial and detrimental role of inflammatory cells in ischemic stroke

Cell type	Detrimental effects	Beneficial effects
Microglia/macrophages	Production of proinflammatory cytokines, including TNF and IL-1, reactive oxygen and nitrogen species, and proteases, such as MMPs. Brain microglia/macrophage phagocytose viable and functional neurons causing brain atrophy.	Resolution of inflammation (IL-10 and TGF-β release, production of arginase, and phagocytic activity). Late reparative processes by producing growth factors (IGF-1, brain-derived neurotrophic factor, and glial cell line-derived neurotrophic factor), production of neurotrophic factors, facilitation of neurogenesis and plasticity, and scavenge and removal necrotic debris
Astrocytes	Production of inflammatory mediators (e.g., TNF-α, IL-1, and MMPs). Edema formation, inhibition of axon regeneration and BBB disruption, glial scar formation, and glutamate release	Extracellular glutamate uptake, synthesis, and release of neurotrophic factors. Glial scar formation, BBB rebuilding, and neurovascular remodeling.
Neutrophils	Microvessel obstruction, ROS production, and release of MMPs that contribute to BBB damage and exacerbate inflammation, stimulation of lipid peroxidation, release of proteolytic enzymes, damage of endothelial cell membrane, increase of BBB permeability, post-ischemic edema, no-reflow phenomenon	N2 phenotype: promote resolution of inflammation
Dendritic cells	Up-regulation of MHC-II and co-stimulatory molecules that prompt the activation of lymphocytes
T Lymphocytes	Facilitate adhesion of platelets and leukocytes to the vascular endothelium causing thromboinflammation and promoting proinflammatory pathways	Interaction of T cells with platelets may also have hemostatic effects preventing hemorrhagic transformation after severe ischemic stroke