Th17 Cell-Mediated Neuroinflammation Is Involved in Neurodegeneration of Aβ1-42-Induced Alzheimer’s Disease Model Rats

• Published in: PloS one Vol. 8; no. 10; p. e75786
• Main Authors: Zhang, Jun, Ke, Kai-Fu, Liu, Zhan, Qiu, Yi-Hua, Peng, Yu-Ping
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 04.10.2013; Public Library of Science (PLoS)
• Subjects: Alzheimer Disease - chemically induced; Alzheimer Disease - immunology; Alzheimer Disease - metabolism; Alzheimer's disease; Amyloid beta-Peptides - toxicity; Amyloid precursor protein; Animals; Apoptosis; Blood circulation; Blood-brain barrier; CD4 antigen; Cerebrospinal fluid; Cytokines; Disease; FasL protein; Female; Gene expression; Gliosis; Helper cells; Hippocampus; Histochemistry; Immune system; Infiltration; Inflammation; Interleukin 22; Interleukin-17 - metabolism; Interleukins - metabolism; Laboratory animals; Latency; Ligands; Lymphocytes; Lymphocytes T; Male; Medicine; Multiple sclerosis; Neurodegeneration; Neurodegenerative Diseases - chemically induced; Neurodegenerative Diseases - immunology; Neurodegenerative Diseases - metabolism; Neurons; Neurotoxicity; Parenchyma; Pathogenesis; Peptide Fragments - toxicity; Peptides; Phosphoprotein phosphatase; Physiology; Protein phosphatase; Proteins; Rats; Rats, Sprague-Dawley; Rodents; Th17 Cells - metabolism; United States > US; China

Neuroinflammation, especially innate immunocyte-mediated neuroinflammation, has been reported to participate in pathogenesis of Alzheimer's disease (AD). However, the involvement of adaptive immune cells, such as CD4(+) T lymphocytes, in pathogenesis of AD is not well clarified. Herein, we focu...