Abstract

The immune response following acute stroke has received significant attention. The spleen is an important immune organ, and more and more studies have shown that brain-spleen crosstalk after stroke plays an important role in its development and prognosis. There are many mechanisms of spleen activation after stroke, including activation of the sympathetic nervous system, the production of chemokines, and antigen presentation in the damaged brain. The changes in the spleen after stroke are mainly reflected in morphology, changes to immune cells, and cytokine production. Once activated, the spleen contracts, undergoes cellular changes, and releases inflammatory cytokines. Some studies have also shown that spleen cells specifically migrate to the site of primary brain injury. The size of the spleen is also negatively correlated with infarct volume — the more serious the spleen atrophy, the larger the infarct volume. Therefore, a comprehensive understanding of the dynamic response of the spleen to stroke will not only enable understanding of the evolution of ischemic brain injury but will also enable the identification of potential targets for stroke treatment. Here, we review recent basic and clinical drug studies on the spleen as a target for the treatment of stroke, focusing on therapeutic strategies for regulating the splenic response and inhibiting secondary brain injury.

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