KIR2DL4-HLAG interaction at human NK cell-oligodendrocyte interfaces regulates IFN-γ-mediated effects.
Cell Line
Cytotoxicity, Immunologic
/ immunology
HLA-G Antigens
/ immunology
Humans
Interferon-gamma
/ immunology
Killer Cells, Natural
/ immunology
Multiple Sclerosis
/ immunology
Myelin-Associated Glycoprotein
/ immunology
Oligodendroglia
/ immunology
Receptors, KIR2DL4
/ immunology
Receptors, Natural Killer Cell
/ immunology
Demyelination
Multiple sclerosis
Myelin protein
Natural killer cell
Oligodendrocyte
Journal
Molecular immunology
ISSN: 1872-9142
Titre abrégé: Mol Immunol
Pays: England
ID NLM: 7905289
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
received:
02
02
2018
revised:
11
09
2018
accepted:
30
09
2018
pubmed:
30
11
2018
medline:
18
1
2020
entrez:
29
11
2018
Statut:
ppublish
Résumé
Interactions between germline-encoded natural killer (NK) cell receptors and their respective ligands on tumorigenic or virus-infected cells determine NK cell cytotoxic activity and/or cytokine secretion. NK cell cytokine responses can be augmented in and can potentially contribute to multiple sclerosis (MS), an inflammatory disease of the central nervous system focused upon the oligodendrocytes (OLs). To investigate mechanisms by which NK cells may contribute to MS pathogenesis, we developed an in vitro human model of OL-NK cell interaction. We found that activated, but not resting human NK cells form conjugates with, and mediate cytotoxicity against, human oligodendrocytes. NK cells, when in conjugate with OLs, rapidly synthesize and polarize IFN-γ toward the OLs. IFN-γ is capable of reducing myelin oligodendrocyte and myelin associated glycoproteins (MOG and MAG) content. This activity is independent of MHC class-I mediated inhibition via KIR2DL1, but dependent upon the interaction between NK cell-expressed KIR2DL4 and its oligodendrocyte-expressed ligand, HLA-G. NK cells from patients with MS express higher levels of IFN-γ following conjugation to OLs, more actively promote in vitro reduction of MOG and MAG and have higher frequencies of the KIR2DL4 positive population. These data collectively suggest a mechanism by which NK cells can promote pathogenic effects upon OLs.
Identifiants
pubmed: 30482463
pii: S0161-5890(18)30835-6
doi: 10.1016/j.molimm.2018.09.027
pmc: PMC6543535
mid: NIHMS1515352
pii:
doi:
Substances chimiques
HLA-G Antigens
0
KIR2DL4 protein, human
0
Myelin-Associated Glycoprotein
0
Receptors, KIR2DL4
0
Receptors, Natural Killer Cell
0
Interferon-gamma
82115-62-6
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
39-55Subventions
Organisme : NCI NIH HHS
ID : P30 CA006927
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI067946
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA100226
Pays : United States
Informations de copyright
Copyright © 2018 Elsevier Ltd. All rights reserved.
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