Exp Neurobiol.  2021 Apr;30(2):101-112. 10.5607/en20033.

Immunosuppression and Neuroinflammation in Stroke Pathobiology

  • 1China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing 101100, China
  • 2Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing 101100, China
  • 3Department of Neurosurgery, Wayne State University School of Medicine, Detroit 48201, MI, USA
  • 4Department of Research & Development Center, John D. Dingell VA Medical Center, Detroit 48201, MI, USA


Over the preceding decades, there have been substantial advances in our knowledge of the pathophysiology of stroke. One such advance has been an increased understanding of the multifarious crosstalk in which the nervous and immune systems engage in order to maintain homeostasis. By interrupting the immune-nervous nexus, it is thought that stroke induces change in both systems. Additionally, it has been found that both innate and adaptive immunosuppression play protective roles against the effects of stroke. The release of danger-/damage-associated molecular patterns (DAMPs) activates Toll-like receptors (TLRs), contributing to the harmful inflammatory effects of ischemia/reperfusion injury after stroke; the Tyro3, Axl, and MerTK (TAM)/Gas6 system, however, has been shown to suppress inflammation via downstream signaling molecules that inhibit TLR signaling. Anti-inflammatory cytokines have also been found to promote neuroprotection following stroke. Additionally, adaptive immunosuppression merits further consideration as a potential endogenous protective mechanism. In this review, we highlight recent studies regarding the effects and mechanism of immunosuppression on the pathophysiology of stroke, with the hope that a better understanding of the function of both of innate and adaptive immunity in this setting will facilitate the development of effective therapies for post-stroke inflammation.


Innate immunity; Anti-inflammatory molecules; Adaptive immunity; Neuro-immunomodulation; Stroke
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