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.