ApoE attenuates unresolvable inflammation by complex formation with activated C1q.
Aged
Aged, 80 and over
Amyloid beta-Peptides
/ immunology
Animals
Antigen-Antibody Complex
/ immunology
Aorta
/ immunology
Apolipoproteins E
/ immunology
Atherosclerosis
/ immunology
Brain
/ immunology
Carotid Arteries
/ immunology
Carotid Artery Diseases
/ immunology
Choroid Plexus
/ immunology
Cognitive Dysfunction
/ immunology
Complement C1q
/ immunology
Complement C5
Complement Pathway, Classical
/ immunology
Female
Humans
Leukocytes
Male
Mice, Knockout, ApoE
Microscopy, Fluorescence
Middle Aged
Plaque, Amyloid
/ immunology
Protein Isoforms
/ immunology
RNA, Small Interfering
Journal
Nature medicine
ISSN: 1546-170X
Titre abrégé: Nat Med
Pays: United States
ID NLM: 9502015
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
18
09
2018
accepted:
13
12
2018
pubmed:
30
1
2019
medline:
14
5
2019
entrez:
30
1
2019
Statut:
ppublish
Résumé
Apolipoprotein-E (ApoE) has been implicated in Alzheimer's disease, atherosclerosis, and other unresolvable inflammatory conditions but a common mechanism of action remains elusive. We found in ApoE-deficient mice that oxidized lipids activated the classical complement cascade (CCC), resulting in leukocyte infiltration of the choroid plexus (ChP). All human ApoE isoforms attenuated CCC activity via high-affinity binding to the activated CCC-initiating C1q protein (K
Identifiants
pubmed: 30692699
doi: 10.1038/s41591-018-0336-8
pii: 10.1038/s41591-018-0336-8
pmc: PMC6420126
mid: EMS80920
doi:
Substances chimiques
Amyloid beta-Peptides
0
Antigen-Antibody Complex
0
ApoE protein, human
0
Apolipoproteins E
0
Complement C5
0
Protein Isoforms
0
RNA, Small Interfering
0
Complement C1q
80295-33-6
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Video-Audio Media
Langues
eng
Sous-ensembles de citation
IM
Pagination
496-506Commentaires et corrections
Type : ErratumIn
Type : CommentIn
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