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CD4+ effector T cells accelerate Alzheimer's disease in mice

J Neuroinflammation. 2021-11; 
Jatin Machhi, Pravin Yeapuri, Yaman Lu, Emma Foster, Rupesh Chikhale, Jonathan Herskovitz, Krista L Namminga, Katherine E Olson, Mai Mohamed Abdelmoaty, Ju Gao, Rolen M Quadros, Tomomi Kiyota, Liang Jingjing, Bhavesh D Kevadiya, Xinglong Wang, Yutong Liu, Larisa Y Poluektova, Channabasavaiah B Gurumurthy, R Lee Mosley, Howard E Gendelman
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Recombinant Proteins CD4+ T cells were enriched from single cell suspensions using an EasySep? mouse CD4+ T cell isolation kit (Catalog No. 19852, Stemcell Technologies) and recovered CD4+ T cells (98% CD4+ by flow cytometric analysis) were cultured in vitro in the presence of monomeric Aβ1–42?(25?μg/ml) prepared as described before [71] (Catalog no. RP10017, GenScript) and 2.5?×?107?feeder cells, Get A Quote

摘要

background: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by pathological deposition of misfolded self-protein amyloid beta (Aβ) which in kind facilitates tau aggregation and neurodegeneration. Neuroinflammation is accepted as a key disease driver caused by innate microglia activation. Recently, adaptive immune alterations have been uncovered that begin early and persist throughout the disease. How these occur and whether they can be harnessed to halt disease progress is unclear. We propose that self-antigens would induct autoreactive effector T cells (Teffs) that drive pro-inflammatory and neurodestructive immunity leading to cognitive impairments. Here, we investigated th... More

關鍵詞

APP/PS1 transgenic mice, Alzheimer’s disease (AD), Amyloid beta (Aβ), Effector T cell (Teff), Regulatory T cell (Treg), T cell
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