Hippocampal T cell infiltration promotes neuroinflammation and cognitive decline in a mouse model of tauopathy. Laurent, C., Dorothée, G., Hunot, S., Martin, E., Monnet, Y., Duchamp, M., Dong, Y., Légeron, F., Leboucher, A., Burnouf, S., Faivre, E., Carvalho, K., Caillierez, R., Zommer, N., Demeyer, D., Jouy, N., Sazdovitch, V., Schraen-Maschke, S., Delarasse, C., Buée, L., & Blum, D. Brain: A Journal of Neurology, 140(1):184–200, January, 2017.
doi  abstract   bibtex   
Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of clinical symptoms. Neuroinflammatory changes are thought to be major contributors to Alzheimer's disease pathophysiology, even if their precise role still remains largely debated. Notably, to what extent immune responses contribute to cognitive impairments promoted by tau pathology remains poorly understood. To address this question, we took advantage of the THY-Tau22 mouse model that progressively develops hippocampal tau pathology paralleling cognitive deficits and reappraised the interrelationship between tau pathology and brain immune responses. In addition to conventional astroglial and microglial responses, we identified a CD8-positive T cell infiltration in the hippocampus of tau transgenic mice associated with an early chemokine response, notably involving CCL3. Interestingly, CD8-positive lymphocyte infiltration was also observed in the cortex of patients exhibiting frontemporal dementia with P301L tau mutation. To gain insights into the functional involvement of T cell infiltration in the pathophysiological development of tauopathy in THY-Tau22 mice, we chronically depleted T cells using anti-CD3 antibody. Such anti-CD3 treatment prevented hippocampal T cell infiltration in tau transgenic animals and reverted spatial memory deficits, in absence of tau pathology modulation. Altogether, these data support an instrumental role of hippocampal T cell infiltration in tau-driven pathophysiology and cognitive impairments in Alzheimer's disease and other tauopathies.
@article{laurent_hippocampal_2017,
	title = {Hippocampal {T} cell infiltration promotes neuroinflammation and cognitive decline in a mouse model of tauopathy},
	volume = {140},
	issn = {1460-2156},
	doi = {10.1093/brain/aww270},
	abstract = {Alzheimer's disease is characterized by the combined presence of amyloid plaques and tau pathology, the latter being correlated with the progression of clinical symptoms. Neuroinflammatory changes are thought to be major contributors to Alzheimer's disease pathophysiology, even if their precise role still remains largely debated. Notably, to what extent immune responses contribute to cognitive impairments promoted by tau pathology remains poorly understood. To address this question, we took advantage of the THY-Tau22 mouse model that progressively develops hippocampal tau pathology paralleling cognitive deficits and reappraised the interrelationship between tau pathology and brain immune responses. In addition to conventional astroglial and microglial responses, we identified a CD8-positive T cell infiltration in the hippocampus of tau transgenic mice associated with an early chemokine response, notably involving CCL3. Interestingly, CD8-positive lymphocyte infiltration was also observed in the cortex of patients exhibiting frontemporal dementia with P301L tau mutation. To gain insights into the functional involvement of T cell infiltration in the pathophysiological development of tauopathy in THY-Tau22 mice, we chronically depleted T cells using anti-CD3 antibody. Such anti-CD3 treatment prevented hippocampal T cell infiltration in tau transgenic animals and reverted spatial memory deficits, in absence of tau pathology modulation. Altogether, these data support an instrumental role of hippocampal T cell infiltration in tau-driven pathophysiology and cognitive impairments in Alzheimer's disease and other tauopathies.},
	language = {eng},
	number = {1},
	journal = {Brain: A Journal of Neurology},
	author = {Laurent, Cyril and Dorothée, Guillaume and Hunot, Stéphane and Martin, Elodie and Monnet, Yann and Duchamp, Marie and Dong, Yuan and Légeron, François-Pierre and Leboucher, Antoine and Burnouf, Sylvie and Faivre, Emilie and Carvalho, Kévin and Caillierez, Raphaëlle and Zommer, Nadège and Demeyer, Dominique and Jouy, Nathalie and Sazdovitch, Veronique and Schraen-Maschke, Susanna and Delarasse, Cécile and Buée, Luc and Blum, David},
	month = jan,
	year = {2017},
	pmid = {27818384},
	pmcid = {PMC5382942},
	keywords = {Aged, Hippocampus, Humans, Cerebral Cortex, Middle Aged, Animals, frontotemporal lobar degeneration, Tauopathies, Mice, Mice, Inbred C57BL, Mice, Transgenic, Disease Models, Animal, Cognitive Dysfunction, tauopathy, CD3 Complex, Antibodies, Inflammation, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, chemokines, Chemokines, neuroinflammation, T cells},
	pages = {184--200}
}
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