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Neuroprotection against ischemic stroke requires a specific class of early responder T cells in mice
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Neuroprotection against ischemic stroke requires a specific class of early responder T cells in mice
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Journal Article
Neuroprotection against ischemic stroke requires a specific class of early responder T cells in mice
2022
Overview
Immunomodulation holds therapeutic promise against brain injuries, but leveraging this approach requires a precise understanding of mechanisms. We report that [CD8.sup.+][CD122.sup.+][CD49d.sup.lo] T regulatory-like cells ([CD8.sup.+] TRLs) are among the earliest lymphocytes to infiltrate mouse brains after ischemic stroke and temper inflammation; they also confer neuroprotection. TRL depletion worsened stroke outcomes, an effect reversed by [CD8.sup.+] TRL reconstitution. The CXCR3/CXCL10 axis served as the brain-homing mechanism for [CD8.sup.+] TRLs. Upon brain entry, [CD8.sup.+] TRLs were reprogrammed to upregulate leukemia inhibitory factor (LIF) receptor, epidermal growth factor-like transforming growth factor (ETGF), and interleukin 10 (IL-10). LIF/LIF receptor interactions induced ETGF and IL-10 production in [CD8.sup.+] TRLs. While IL-10 induction was important for the Anti-inflammatory effects of [CD8.sup.+] TRLs, ETGF provided direct neuroprotection. Poststroke intravenous transfer of [CD8.sup.+] TRLs reduced infarction, promoting long-term neurological recovery in young males or aged mice of both sexes. Thus, these unique [CD8.sup.+] TRLs serve as early responders to rally defenses against stroke, offering fresh perspectives for clinical translation.
