Regulatory T cells(Tregs)constitute a subset of T cells that play a protective role by suppressing inflammation[1].We previously documented that the Treg immu-nomodulatory mechanisms are compromised in AD patients[2],...Regulatory T cells(Tregs)constitute a subset of T cells that play a protective role by suppressing inflammation[1].We previously documented that the Treg immu-nomodulatory mechanisms are compromised in AD patients[2],resulting in an activation of peripheral monocytes,associated with upregulation of inflamma-tory mediators[3].Preclinical studies have suggested variable effects of Treg modification on the neurode-generative process.While some studies propose that the Treg population might obstruct a selective gateway for immune cell trafficking to the CNS,thereby compromis-ing reparative immune responses[4,5],an increasing number of preclinical studies,including ours,indicate that systemic Treg expansion through interleukine-2(IL-2)administration or ex vivo expanded Treg administra-tion effectively modulates neuroinflammation and allevi-ates AD pathology[6,7].IL-2,originally described as the main T-cell growth factor,has been used in standard high doses for activation of cytotoxic T cells and NK cells[8].展开更多
基金supported by the Alzheimer’s Association Part-The-Cloud Award,the Houston Methodist Clinical Scholar Award and a fund from MD Anderson Foundation.
文摘Regulatory T cells(Tregs)constitute a subset of T cells that play a protective role by suppressing inflammation[1].We previously documented that the Treg immu-nomodulatory mechanisms are compromised in AD patients[2],resulting in an activation of peripheral monocytes,associated with upregulation of inflamma-tory mediators[3].Preclinical studies have suggested variable effects of Treg modification on the neurode-generative process.While some studies propose that the Treg population might obstruct a selective gateway for immune cell trafficking to the CNS,thereby compromis-ing reparative immune responses[4,5],an increasing number of preclinical studies,including ours,indicate that systemic Treg expansion through interleukine-2(IL-2)administration or ex vivo expanded Treg administra-tion effectively modulates neuroinflammation and allevi-ates AD pathology[6,7].IL-2,originally described as the main T-cell growth factor,has been used in standard high doses for activation of cytotoxic T cells and NK cells[8].
