Role of Chemokine Receptor CCR4 and Regulatory T Cells in Wound Healing of Diabetic Mice.
Alloxan
/ pharmacology
Analysis of Variance
Animals
Biopsy, Needle
Chemokine CCL17
/ antagonists & inhibitors
Chemokine CCL22
/ antagonists & inhibitors
Chemokines
/ metabolism
Diabetes Mellitus, Experimental
/ metabolism
Diabetes Mellitus, Type 1
/ drug therapy
Humans
Immunohistochemistry
Mice
Mice, Inbred C57BL
Mice, Knockout
Real-Time Polymerase Chain Reaction
/ methods
Receptors, CCR4
/ metabolism
Wound Healing
/ drug effects
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
08
03
2018
revised:
14
09
2018
accepted:
02
10
2018
pubmed:
23
11
2018
medline:
8
5
2020
entrez:
23
11
2018
Statut:
ppublish
Résumé
Wound healing is a well-coordinated process that involves inflammatory mediators and cellular responses; however, if any disturbances are present during this process, tissue repair is impaired. Chronic wounds are one of the serious long-term complications associated with diabetes mellitus. The chemokine receptor CCR4 and its respective ligands, CCL17 and CCL22, are involved in regulatory T cell recruitment and activation in inflamed skin; however, the role of regulatory T cells in wounds is still not clear. Our aim was to investigate the role of CCR4 and regulatory T cells in cutaneous wound healing in diabetic mice. Alloxan-induced diabetic wild- type mice (diabetic) developed wounds that were difficult to heal, differently from CCR4
Identifiants
pubmed: 30465800
pii: S0022-202X(18)32823-9
doi: 10.1016/j.jid.2018.10.039
pii:
doi:
Substances chimiques
Chemokine CCL17
0
Chemokine CCL22
0
Chemokines
0
Receptors, CCR4
0
Alloxan
6SW5YHA5NG
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1161-1170Informations de copyright
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.