Fig. 9

Stem cell therapy enhances recovery after stroke. In the untreated scenario, ischaemic stroke leads to activation of the peripheral immune system. During this process, the spleen atrophies, lymphocytes undergo apoptosis in the spleen, the inflammatory factor levels in the spleen increase, and inflammatory cells are released from the spleen into circulation. The antigen presentation of DCs is enhanced, and the levels of various chemokines are elevated. These pro-inflammatory mediators contribute to M1 microglia-mediated destruction of the BBB and CNS inflammation. Infiltration of leukocytes further aggravates inflammatory necrosis of neurons. Intravenous administration of stem cells reverses splenic atrophy and converts macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype and Th cells from the pro-inflammatory Th1 phenotype to the anti-inflammatory Th2 phenotype. The inflammatory cytokine and cell levels in the spleen decrease, and anti-inflammatory cytokines and cells begin to be produced and released into circulation, which ultimately lead to less BBB restructuring and CNS inflammation and provide a favourable environment for nerve regeneration and angiogenesis