Systemic immune‐checkpoint blockade with anti‐PD1 antibodies does not alter cerebral amyloid‐β burden in several amyloid transgenic mouse models

Chronic inflammation represents a central component in the pathogenesis of Alzheimer's disease (AD). Recent work suggests that breaking immune tolerance by Programmed cell Death‐1 (PD1) checkpoint inhibition produces an IFN‐γ‐dependent systemic immune response, with infiltration of the brain by...

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Veröffentlicht in:	Glia 2018-03, Vol.66 (3), p.492-504
Hauptverfasser:	Latta‐Mahieu, Martine, Elmer, Bradford, Bretteville, Alexis, Wang, Yaming, Lopez‐Grancha, Mati, Goniot, Philippe, Moindrot, Nicolas, Ferrari, Paul, Blanc, Véronique, Schussler, Nathalie, Brault, Emmanuel, Roudières, Valérie, Blanchard, Véronique, Yang, Zhi‐Yong, Barneoud, Pascal, Bertrand, Philippe, Roucourt, Bart, Carmans, Sofie, Bottelbergs, Astrid, Mertens, Liesbeth, Wintmolders, Cindy, Larsen, Peter, Hersley, Caroline, McGathey, Tyler, Racke, Margaret M., Liu, Ling, Lu, Jirong, O'Neill, Michael J., Riddell, David R., Ebneth, Andreas, Nabel, Gary J., Pradier, Laurent
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - immunology Alzheimer Disease - pathology Alzheimer Disease - therapy Alzheimer's Disease amyloid Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Animals Antibodies - administration & dosage Antibodies - metabolism Brain - immunology Brain - pathology checkpoint inhibition Disease Models, Animal Female Humans Immunohistochemistry Immunotherapy Interferon-gamma - blood Male Mice, Inbred C57BL Mice, Transgenic Presenilin-1 - genetics Presenilin-1 - metabolism Programmed Cell Death 1 Receptor - immunology Random Allocation RNA, Messenger - metabolism Spleen - immunology
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