TY - JOUR
T1 - PD-1/PD-L1 checkpoint blockade harnesses monocyte-derived macrophages to combat cognitive impairment in a tauopathy mouse model
AU - Rosenzweig, Neta
AU - Dvir-Szternfeld, Raz
AU - Tsitsou-Kampeli, Afroditi
AU - Keren-Shaul, Hadas
AU - Ben-Yehuda, Hila
AU - Weill-Raynal, Pierre
AU - Cahalon, Liora
AU - Kertser, Alex
AU - Baruch, Kuti
AU - Amit, Ido
AU - Weiner, Assaf
AU - Schwartz, Michal
N1 - We thank Prof. Dan Frenkel (Tel-Aviv University, Israel) for his generous gift of DM-hTAU and MSR1−/− mice and Dr. Shelley Schwarzbaum for editing the manuscript. Research in the M.S. lab is supported by Advanced European Research Council grants (232835), and by the EU Seventh Framework Program HEALTH-2011 (279017); Israel Science Foundation (ISF)-research grant no. 991/16; and ISF-Legacy Heritage Biomedical Science Partnership-research grant no. 1354/15. We wish to thank the Adelis Foundation for their generous support of our AD research. M.S. holds the Maurice and Ilse Katz Professorial Chair in Neuroimmunology. All listed authors were either students or employees at the Weizmann Institute of Science while conducting their work.
PY - 2019/1/28
Y1 - 2019/1/28
N2 - Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies. Harnessing the immune system by blocking the programmed cell death receptor (PD)-1 pathway in an amyloid beta mouse model was shown to evoke a sequence of immune responses that lead to disease modification. Here, blocking PD-L1, a PD-1 ligand, was found to have similar efficacy to that of PD-1 blocking in disease modification, in both animal models of AD and of tauopathy. Targeting PD-L1 in a tau-driven disease model resulted in increased immunomodulatory monocyte-derived macrophages within the brain parenchyma. Single cell RNA-seq revealed that the homing macrophages expressed unique scavenger molecules including macrophage scavenger receptor 1 (MSR1), which was shown here to be required for the effect of PD-L1 blockade in disease modification. Overall, our results demonstrate that immune checkpoint blockade targeting the PD-1/PD-L1 pathway leads to modification of common factors that go awry in AD and dementia, and thus can potentially provide an immunotherapy to help combat these diseases.
AB - Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies. Harnessing the immune system by blocking the programmed cell death receptor (PD)-1 pathway in an amyloid beta mouse model was shown to evoke a sequence of immune responses that lead to disease modification. Here, blocking PD-L1, a PD-1 ligand, was found to have similar efficacy to that of PD-1 blocking in disease modification, in both animal models of AD and of tauopathy. Targeting PD-L1 in a tau-driven disease model resulted in increased immunomodulatory monocyte-derived macrophages within the brain parenchyma. Single cell RNA-seq revealed that the homing macrophages expressed unique scavenger molecules including macrophage scavenger receptor 1 (MSR1), which was shown here to be required for the effect of PD-L1 blockade in disease modification. Overall, our results demonstrate that immune checkpoint blockade targeting the PD-1/PD-L1 pathway leads to modification of common factors that go awry in AD and dementia, and thus can potentially provide an immunotherapy to help combat these diseases.
UR - http://www.scopus.com/inward/record.url?scp=85060630289&partnerID=8YFLogxK
U2 - 10.1038/s41467-019-08352-5
DO - 10.1038/s41467-019-08352-5
M3 - مقالة
SN - 2041-1723
VL - 10
JO - Nature Communications
JF - Nature Communications
IS - 1
M1 - 465
ER -