ICOSL Stimulation by ICOS-Fc Accelerates Cutaneous Wound Healing In Vivo.


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:
01 Jul 2022
Historique:
received: 01 06 2022
revised: 29 06 2022
accepted: 30 06 2022
entrez: 9 7 2022
pubmed: 10 7 2022
medline: 14 7 2022
Statut: epublish

Résumé

ICOS and its ligand ICOSL are immune receptors whose interaction triggers bidirectional signals that modulate the immune response and tissue repair. The aim of this study was to assess the in vivo effects of ICOSL triggering by ICOS-Fc, a recombinant soluble form of ICOS, on skin wound healing. The effect of human ICOS-Fc on wound healing was assessed, in vitro, and, in vivo, by skin wound healing assay using ICOS We show that, in wild type mice, treatment with ICOS-Fc improves wound healing, promotes angiogenesis, preceded by upregulation of IL-6 and VEGF expression; increases the number of fibroblasts and T cells, whereas it reduces that of neutrophils; and increases the number of M2 vs. M1 macrophages. Fittingly, ICOS-Fc enhanced M2 macrophage migration, while it hampered that of M1 macrophages. ICOS These data show that the ICOS/ICOSL network cooperates in tissue repair, and that triggering of ICOSL by ICOS-Fc improves cutaneous wound healing by increasing angiogenesis and recruitment of reparative macrophages.

Sections du résumé

BACKGROUND BACKGROUND
ICOS and its ligand ICOSL are immune receptors whose interaction triggers bidirectional signals that modulate the immune response and tissue repair.
AIM OBJECTIVE
The aim of this study was to assess the in vivo effects of ICOSL triggering by ICOS-Fc, a recombinant soluble form of ICOS, on skin wound healing.
METHODS METHODS
The effect of human ICOS-Fc on wound healing was assessed, in vitro, and, in vivo, by skin wound healing assay using ICOS
RESULTS RESULTS
We show that, in wild type mice, treatment with ICOS-Fc improves wound healing, promotes angiogenesis, preceded by upregulation of IL-6 and VEGF expression; increases the number of fibroblasts and T cells, whereas it reduces that of neutrophils; and increases the number of M2 vs. M1 macrophages. Fittingly, ICOS-Fc enhanced M2 macrophage migration, while it hampered that of M1 macrophages. ICOS
CONCLUSION CONCLUSIONS
These data show that the ICOS/ICOSL network cooperates in tissue repair, and that triggering of ICOSL by ICOS-Fc improves cutaneous wound healing by increasing angiogenesis and recruitment of reparative macrophages.

Identifiants

pubmed: 35806368
pii: ijms23137363
doi: 10.3390/ijms23137363
pmc: PMC9266942
pii:
doi:

Substances chimiques

Icos protein, mouse 0
Icosl protein, mouse 0
Immunoglobulin Fc Fragments 0
Inducible T-Cell Co-Stimulator Ligand 0
Inducible T-Cell Co-Stimulator Protein 0
Recombinant Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Italian Association for Cancer Research
ID : IG 20714
Organisme : Fondazione Cariplo
ID : (2017-0535)
Organisme : University of Turin fund
ID : (DIAC_RILO_21)

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Auteurs

Ian Stoppa (I)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
NOVAICOS srls, 28100 Novara, Italy.

Casimiro Luca Gigliotti (CL)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
NOVAICOS srls, 28100 Novara, Italy.

Nausicaa Clemente (N)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.

Deepika Pantham (D)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
NOVAICOS srls, 28100 Novara, Italy.

Chiara Dianzani (C)

Department of Scienza e Tecnologia del Farmaco, University of Turin, 10124 Turin, Italy.

Chiara Monge (C)

Department of Scienza e Tecnologia del Farmaco, University of Turin, 10124 Turin, Italy.

Chiara Puricelli (C)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
Maggiore della Carità University Hospital, 28100 Novara, Italy.

Roberta Rolla (R)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
Maggiore della Carità University Hospital, 28100 Novara, Italy.

Salvatore Sutti (S)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.

Filippo Renò (F)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.

Renzo Boldorini (R)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
Maggiore della Carità University Hospital, 28100 Novara, Italy.

Elena Boggio (E)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
NOVAICOS srls, 28100 Novara, Italy.

Umberto Dianzani (U)

Department of Health Sciences and Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Università del Piemonte Orientale, 28100 Novara, Italy.
Maggiore della Carità University Hospital, 28100 Novara, Italy.

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