Perspective Review of Myeloid Immune Cell Responses and Poststroke Immunosuppression

Ischemic stroke profoundly influences the peripheral immune system, which responds quickly to brain ischemia and participates in the evolution of poststroke neuroinflammation, while a period of systemic immunosuppression ensues. Poststroke immunosuppression brings harmful consequences, including increased infection rates and escalated death. As the most abundant cell population in the fast-responding innate immune system, myeloid cells including neutrophils and monocytes play an indispensable role in systemic immunosuppression after stroke. The change in myeloid response after stroke can be regulated by circulating DAMPs (damage-associated molecular patterns) and neuromodulatory mechanisms, which contain sympathetic nervous system, hypothalamic-pituitary-adrenal, and parasympathetic nervous system. In this review, we summarize the emerging roles and newly identified mechanisms underlying myeloid cell response in poststroke immunosuppression. Deeper understanding of the above points may pave the way for future development of novel therapeutic strategies to treat poststroke immunosuppression.

Automated summary

Ischemic stroke has a profound impact on the peripheral immune system, leading to rapid brain ischemia response and the development of poststroke neuroinflammation, accompanied by a period of systemic immunosuppression. Myeloid cells, including neutrophils and monocytes, play a crucial role in poststroke immunosuppression as the most abundant cell population in the fast-responding innate immune system. The change in myeloid response after stroke can be regulated by circulating DAMPs and neuromodulatory mechanisms involving the sympathetic nervous system, hypothalamic-pituitary-adrenal axis, and parasympathetic nervous system. This review summarizes the emerging roles and newly identified mechanisms underlying myeloid cell response in poststroke immunosuppression. A deeper understanding of these points may facilitate the development of novel therapeutic strategies for poststroke immunosuppression.