AUTHOR=Wang Shuai , Shi Yubin , Zhang Yanqi , Yuan Fengyun , Mao Mintao , Ma Jun 

TITLE=Tregs depletion aggravates activation of astrocytes by modulating IL-10/GXP4 following cerebral infarction

JOURNAL=Frontiers in Immunology

VOLUME=14

YEAR=2023

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1255316

DOI=10.3389/fimmu.2023.1255316

ISSN=1664-3224

ABSTRACT=<sec><title>Background</title><p>Tregs plays a critical role in the development of secondary injuries in diseases. Accumulating evidence suggests an association between ischemic stroke and renal dysfunction; however, the underlying mechanisms remain unclear. This study aimed to investigate the potential of Tregs in inhibiting the activation of astrocytes after focal cerebral infarction.</p></sec><sec><title>Methods</title><p>This study aimed to investigate the renal consequences of focal cerebral ischemia by subjecting a mouse model to transient middle cerebral artery occlusion (tMCAO). Subsequently, we assessed renal fibrosis, renal ferroptosis, Treg infiltration, astrocyte activation, as well as the expression levels of active GPX4, FSP1, IL-10, IL-6, and IL-2 after a 2-week period.</p></sec><sec><title>Results</title><p>In the tMCAO mouse model, depletion of tregs protected against activation of astrocyte and significantly decreased FSP1, IL-6, IL-2, and NLRP3 expression levels, while partially reversing the changes in Tregs. Mechanistically, tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.</p></sec><sec><title>Conclusion</title><p>Tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.</p></sec>