Trial Registration:May 11th,2018 ClinicalTrials.gov Identifier:NCT03522129 https://clini caltr ials.gov/ct2/show/NCT03522129.Investigational therapies for Alzheimer’s disease(AD)target a wide range of mechanisms,yet ...Trial Registration:May 11th,2018 ClinicalTrials.gov Identifier:NCT03522129 https://clini caltr ials.gov/ct2/show/NCT03522129.Investigational therapies for Alzheimer’s disease(AD)target a wide range of mechanisms,yet promising dis-ease-modifying therapies remain a huge unmet need.Much evidence indicates that the oligomeric form of amyloid-beta(Aβ)is a toxic species contributing to AD through synaptic damage and neuronal toxicity[1].展开更多
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 grants from the National Institute on Aging(AG057780 to SMC)and by Cognition Therapeutics,Inc.
文摘Trial Registration:May 11th,2018 ClinicalTrials.gov Identifier:NCT03522129 https://clini caltr ials.gov/ct2/show/NCT03522129.Investigational therapies for Alzheimer’s disease(AD)target a wide range of mechanisms,yet promising dis-ease-modifying therapies remain a huge unmet need.Much evidence indicates that the oligomeric form of amyloid-beta(Aβ)is a toxic species contributing to AD through synaptic damage and neuronal toxicity[1].
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].
