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Background  Neuroinflammation plays a key role in intracerebral hemorrhage ( ICH )–induced secondary brain injury, but the specific roles of peripheral inflammatory cells such as macrophages and lymphocytes remain unknown. The purpose of this study was to explore the roles of macrophages, T lymphocytes, and the cytokines they secrete as potential targets for treating secondary brain injury after  ICH .    Methods and Results  Our results showed that peripheral macrophages and T lymphocytes successively infiltrated the brain, with macrophage counts peaking 1 day after  ICH  and T‐lymphocyte counts peaking after 4 days. These peaks in cellular infiltration corresponded to increases in interleukin ( IL )‐23 and  IL ‐17 expression, respectively. We found that hemoglobin from the hematoma activated  IL ‐23 secretion by infiltrating macrophages by inducing the formation of toll‐like receptor (TLR) 2/4 heterodimer. This increased  IL ‐23 expression stimulated γδT‐cell production of  IL ‐17, which increased brain edema and neurologic deficits in the model mice as a proinflammatory factor. Finally, we found that sparstolonin B (SsnB) could ameliorate brain edema and neurologic deficits in  ICH  model mice via inhibition of  TLR 2/ TLR 4 heterodimer formation, and notably, SsnB interacted with myeloid differentiation factor 88 Arg196.    Conclusions  Together, our results reveal the importance of the  IL ‐23/ IL ‐17 inflammatory axis in secondary brain injury after  ICH  and thus provide a new therapeutic target for  ICH  treatment.

journal of the american heart association

Interleukin‐23 Secreted by Activated Macrophages Drives γδT Cell Production of Interleukin‐17 to Aggravate Secondary Injury After Intracerebral Hemorrhage