The Cutaneous Wound Innate Immunological Microenvironment.
Adaptive Immunity
Alarmins
/ genetics
Animals
Blood Platelets
/ immunology
Extracellular Traps
Host Microbial Interactions
/ immunology
Humans
Immunity, Innate
Macrophages
/ immunology
Microbiota
/ immunology
Neutrophils
/ immunology
Pathogen-Associated Molecular Pattern Molecules
/ immunology
Regeneration
/ genetics
Skin
/ immunology
Toll-Like Receptors
/ genetics
Wound Healing
/ genetics
Wounds, Nonpenetrating
/ genetics
innate immunity
skin
wounding
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
19 Nov 2020
19 Nov 2020
Historique:
received:
26
10
2020
revised:
17
11
2020
accepted:
17
11
2020
entrez:
24
11
2020
pubmed:
25
11
2020
medline:
5
3
2021
Statut:
epublish
Résumé
The skin represents the first line of defense and innate immune protection against pathogens. Skin normally provides a physical barrier to prevent infection by pathogens; however, wounds, microinjuries, and minor barrier impediments can present open avenues for invasion through the skin. Accordingly, wound repair and protection from invading pathogens are essential processes in successful skin barrier regeneration. To repair and protect wounds, skin promotes the development of a specific and complex immunological microenvironment within and surrounding the disrupted tissue. This immune microenvironment includes both innate and adaptive processes, including immune cell recruitment to the wound and secretion of extracellular factors that can act directly to promote wound closure and wound antimicrobial defense. Recent work has shown that this immune microenvironment also varies according to the specific context of the wound: the microbiome, neuroimmune signaling, environmental effects, and age play roles in altering the innate immune response to wounding. This review will focus on the role of these factors in shaping the cutaneous microenvironment and how this ultimately impacts the immune response to wounding.
Identifiants
pubmed: 33228152
pii: ijms21228748
doi: 10.3390/ijms21228748
pmc: PMC7699544
pii:
doi:
Substances chimiques
Alarmins
0
Pathogen-Associated Molecular Pattern Molecules
0
Toll-Like Receptors
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIGMS NIH HHS
ID : T32 GM007171
Pays : United States
Organisme : NIH HHS
ID : R01AI139207
Pays : United States
Organisme : Duke University
ID : Physician Strong-Start Award
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