c-Kit-positive ILC2s exhibit an ILC3-like signature that may contribute to IL-17-mediated pathologies.
Cells, Cultured
Humans
Interleukin-17
/ immunology
Interleukin-1beta
/ immunology
Interleukin-23 Subunit p19
/ immunology
Interleukin-4
/ immunology
Lymphocytes
/ cytology
Nuclear Receptor Subfamily 1, Group F, Member 3
/ metabolism
Proto-Oncogene Proteins c-kit
/ metabolism
Psoriasis
/ immunology
Receptors, CCR10
/ metabolism
Skin
/ immunology
Transforming Growth Factor beta
/ metabolism
Journal
Nature immunology
ISSN: 1529-2916
Titre abrégé: Nat Immunol
Pays: United States
ID NLM: 100941354
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
22
05
2018
accepted:
15
05
2019
pubmed:
3
7
2019
medline:
20
11
2019
entrez:
3
7
2019
Statut:
ppublish
Résumé
Here we identify a group 2 innate lymphoid cell (ILC2) subpopulation that can convert into interleukin-17 (IL-17)-producing NKp44
Identifiants
pubmed: 31263279
doi: 10.1038/s41590-019-0423-0
pii: 10.1038/s41590-019-0423-0
doi:
Substances chimiques
CCR10 protein, human
0
IL17A protein, human
0
IL1B protein, human
0
IL23A protein, human
0
IL4 protein, human
0
Interleukin-17
0
Interleukin-1beta
0
Interleukin-23 Subunit p19
0
Nuclear Receptor Subfamily 1, Group F, Member 3
0
RORC protein, human
0
Receptors, CCR10
0
Transforming Growth Factor beta
0
Interleukin-4
207137-56-2
KIT protein, human
EC 2.7.10.1
Proto-Oncogene Proteins c-kit
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
992-1003Commentaires et corrections
Type : ErratumIn