Resolution of inflammation and tissue repair. : The immunology of stroke: from mechanisms to transla
Clearing of dead cells and suppression of inflammation are key events in brain repair. Find-me signals (UTP, ATP) attract microglia and macrophages through P2Y2 receptors. Eat-me signals include UDP, which acts on P2Y6 receptors to stimulate microglial phagocytosis
112, and phosphatidylserine (PtdSer), which is translocated to the outer leaflet of the plasma membrane of apoptotic cells
112. PtdSer-binding proteins involved in the clearance of dead cells include milk fat globule epidermal growth factor 8 protein on microglia
113 and T cell immunoglobulin and mucin domain-containing molecule 4 (TIM4) on macrophages
112. Immunoglobulins directed against CNS antigens, which appear after stroke (
Table 2), may also promote phagocytosis by engaging Fc receptors on phagocytic cells. Phagocytosis promotes secretion of IL-10 and TGF-β
56, which, in turn, suppress antigen presentation, promote T
reg formation, inhibit expression of adhesion molecules in endothelial cells and production of proinflammatory cytokines
61. TGF-β and IL-10 are also neuroprotective
114, 115 and may facilitate brain repair processes. In addition, lipoxins, resolvins and protectins, metabolites of arachidonic acid and omega-3 fatty acids that play an active part in the resolution of inflammation in other organs
55, could also contribute to suppress post-ischemic inflammation. Growth factors and MMPs produced by endothelial cells, neurons, astrocytes, oligodendrocytes and microglia are key molecules driving tissue reorganization and repair
63, 116.
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