The C-type Lectin Receptor CLEC12A Recognizes Plasmodial Hemozoin and Contributes to Cerebral Malaria Development.
Animals
CD8-Positive T-Lymphocytes
/ immunology
Cross-Priming
Dendritic Cells
/ immunology
Disease Models, Animal
Granzymes
/ metabolism
Hemeproteins
/ immunology
Immunity, Innate
Lectins, C-Type
/ genetics
Malaria, Cerebral
/ immunology
Mice
Mice, Inbred C57BL
Plasmodium berghei
/ pathogenicity
Receptors, Mitogen
/ genetics
T-Lymphocytes
C-type lectin receptor
MICL/CLEC12A
Plasmodium berghei
cerebral malaria
hemozoin
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
02 07 2019
02 07 2019
Historique:
received:
05
09
2017
revised:
15
03
2019
accepted:
04
06
2019
entrez:
4
7
2019
pubmed:
4
7
2019
medline:
28
8
2020
Statut:
ppublish
Résumé
Malaria represents a major cause of death from infectious disease. Hemozoin is a Plasmodium-derived product that contributes to progression of cerebral malaria. However, there is a gap of knowledge regarding how hemozoin is recognized by innate immunity. Myeloid C-type lectin receptors (CLRs) encompass a family of carbohydrate-binding receptors that act as pattern recognition receptors in innate immunity. In the present study, we identify the CLR CLEC12A as a receptor for hemozoin. Dendritic cell-T cell co-culture assays indicate that the CLEC12A/hemozoin interaction enhances CD8
Identifiants
pubmed: 31269448
pii: S2211-1247(19)30781-8
doi: 10.1016/j.celrep.2019.06.015
pmc: PMC6616648
pii:
doi:
Substances chimiques
CLEC12A protein, human
0
CLEC12A protein, mouse
0
Hemeproteins
0
Lectins, C-Type
0
Receptors, Mitogen
0
hemozoin
39404-00-7
Granzymes
EC 3.4.21.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
30-38.e5Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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