Constitutive Expression of CCL22 Is Mediated by T Cell-Derived GM-CSF.
Animals
CD11 Antigens
/ genetics
Chemokine CCL22
/ genetics
Dendritic Cells
/ cytology
Gene Expression Regulation
/ immunology
Gonadotropin-Releasing Hormone
/ analogs & derivatives
Granulocyte-Macrophage Colony-Stimulating Factor
/ genetics
Mice, Knockout
T-Lymphocytes, Regulatory
/ cytology
Th2 Cells
/ cytology
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
15 10 2020
15 10 2020
Historique:
received:
03
01
2020
accepted:
06
08
2020
pubmed:
11
9
2020
medline:
30
3
2021
entrez:
10
9
2020
Statut:
ppublish
Résumé
CCL22 is a key mediator of leukocyte trafficking in inflammatory immune responses, allergy, and cancer. It acts by attracting regulatory T cells and Th2 cells via their receptor CCR type 4 (CCR4). Beyond its role in inflammation, CCL22 is constitutively expressed at high levels in lymphoid organs during homeostasis, where it controls immunity by recruiting regulatory T cells to dendritic cells (DCs). In this study, we aimed to identify the mechanisms responsible for constitutive CCL22 expression. We confirmed that CD11c
Identifiants
pubmed: 32907996
pii: jimmunol.2000004
doi: 10.4049/jimmunol.2000004
doi:
Substances chimiques
CD11 Antigens
0
Ccl22 protein, mouse
0
Chemokine CCL22
0
Itgax protein, mouse
0
Gonadotropin-Releasing Hormone
33515-09-2
Granulocyte-Macrophage Colony-Stimulating Factor
83869-56-1
MI 1544
87565-51-3
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2056-2065Informations de copyright
Copyright © 2020 by The American Association of Immunologists, Inc.