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Published on: November 9, 2018
The Role of T Cells in Alzheimer's Disease Pathogenesis
Jin Zhao1, Xiaofang Wang2, Yusheng He3
1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University, and Guangdong Provincial Key Laboratory of Single Cell Technology and Application, Guangzhou, Guangdong, 510515, China; ZhuHai Hengqin ImStem Biotechnology Co. Ltd., Hengqin New District Huandao Donglu 1889 Building 3, Zhuhai, Guangdong, 519000, China; Key Laboratory of Mental Health of the Ministry of Education, Guangdong Province Key Laboratory of Psychiatric Disorders, School of Basic Medical Sciences, Southern Medical University, Guangdong, 510515, China.
Abstract:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with memory decline and cognitive impairment, which is related to hallmark protein aggregates, amyloid-β (Аβ) plaques and neurofibrillary tangles; the latter are accumulated with hyperphosphorylated Tau protein. Immune cells play an important role in AD pathogenesis. Although the role of T cells in AD remains controversial, studies have shown that T cell deficiency is associated with increased AD pathology. In contrast, transplantation of T cells reduces AD pathology. T cells can help B cells generate anti-Аβ antibody to neutralize the toxin of Аβ and hyperphosphorylated Tau. T cells also activate macrophages to phagocytose misfolded proteins including Аβ and Tau. Recent data have also shown that AD animals have a damaged thymic microenvironment, especially thymic epithelial cells (TECs), resulting in decreased T cell numbers, which contribute to AD pathology. Therefore, regulation of T cell regeneration, for example by rejuvenating the thymic microenvironment, has the potential to be used in the treatment of AD.
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