Fig. 3
From: The spleen may be an important target of stem cell therapy for stroke
Inflammation after stroke. DAMPs released from necrotic neurons activate macrophages through PRRs and the inflammasome. Activated macrophages enhance inflammation by releasing pro-inflammatory cytokines and recruiting T cells, which contribute to maintenance of inflammation through IL-17. DCs also activate and enhance antigen presentation to T cells. Gelatinase released by activated mast cells and MPP-9 produced by infiltrating neutrophils destroy the function of the BBB, resulting in brain oedema. Then, under the action of chemokines, leukocytes infiltrate into the damaged brain tissue, thereby expanding inflammation and injury. Several days after acute stroke, the cytokines produced by the innate immune system change to an anti-inflammatory phenotype, which contributes to inhibition of inflammation. The ratio and biodistribution of M1 and M2 microglia also changes, with anti-inflammatory M2 microglia becoming dominant again. Debris is cleaned up by microglia and macrophages. NSCs/NPCs are mobilised and migrate to the lesion. The environment becomes conducive to nerve regeneration, angiogenesis and BBB restructuring