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@ARTICLE{Schlepckow:151484,
author = {Schlepckow, Kai and Monroe, Kathryn M and Kleinberger,
Gernot and Cantuti-Castelvetri, Ludovico and Parhizkar,
Samira and Xia, Dan and Willem, Michael and Werner, Georg
and Pettkus, Nadine and Brunner, Bettina and Sülzen, Alice
and Nuscher, Brigitte and Hampel, Heike and Xiang, Xianyuan
and Feederle, Regina and Tahirovic, Sabina and Park, Joshua
I and Prorok, Rachel and Mahon, Cathal and Liang, Chun‐Chi
and Shi, Ju and Kim, Do Jin and Sabelström, Hanna and
Huang, Fen and Di Paolo, Gilbert and Simons, Mikael and
Lewcock, Joseph W and Haass, Christian},
title = {{E}nhancing protective microglial activities with a dual
function {TREM} 2 antibody to the stalk region},
journal = {EMBO molecular medicine},
volume = {12},
number = {4},
issn = {1757-4676},
address = {Heidelberg},
publisher = {EMBO Press},
reportid = {DZNE-2020-01072},
pages = {e11227},
year = {2020},
abstract = {Triggering receptor expressed on myeloid cells 2 (TREM2) is
essential for the transition of homeostatic microglia to a
disease‐associated microglial state. To enhance TREM2
activity, we sought to selectively increase the
full‐length protein on the cell surface via reducing its
proteolytic shedding by A Disintegrin And Metalloproteinase
(i.e., α‐secretase) 10/17. We screened a panel of
monoclonal antibodies against TREM2, with the aim to
selectively compete for α‐secretase‐mediated shedding.
Monoclonal antibody 4D9, which has a stalk region epitope
close to the cleavage site, demonstrated dual mechanisms of
action by stabilizing TREM2 on the cell surface and reducing
its shedding, and concomitantly activating phospho‐SYK
signaling. 4D9 stimulated survival of macrophages and
increased microglial uptake of myelin debris and amyloid
β‐peptide in vitro. In vivo target engagement was
demonstrated in cerebrospinal fluid, where nearly all
soluble TREM2 was 4D9‐bound. Moreover, in a mouse model
for Alzheimer's disease‐related pathology, 4D9 reduced
amyloidogenesis, enhanced microglial TREM2 expression, and
reduced a homeostatic marker, suggesting a protective
function by driving microglia toward a disease‐associated
state.},
keywords = {Amyloid beta-Peptides / Animals / Antibodies, Monoclonal:
pharmacology / Cell Line, Tumor / Female / Macrophages /
Membrane Glycoproteins: immunology / Mice / Microglia:
pathology / Multiple Myeloma / Rats / Rats, Wistar /
Receptors, Immunologic: immunology},
cin = {AG Haass / Core Technical Staff / AG Tahirovic},
ddc = {610},
cid = {I:(DE-2719)1110007 / I:(DE-2719)1340007 /
I:(DE-2719)1140003},
pnm = {341 - Molecular Signaling (POF3-341) / 342 - Disease
Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC7136959},
pubmed = {pmid:32154671},
doi = {10.15252/emmm.201911227},
url = {https://pub.dzne.de/record/151484},
}