The role of lymphocytes in wound healing

Martin, C J; Muir, I.F.K.

doi:10.1016/0007-1226(90)90185-3

Cited by 98 publications

(73 citation statements)

References 5 publications

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“…However, when the ratio of Mfs to T cells is high, IFN-g-induced Mfs exhibit anti-inflammatory properties, because the resulting NO is sufficient to suppress local T cell proliferation. This situation is physiologically relevant both in sites of acute infection (e.g., wounds) and in noninfected tissues, where Mfs are more abundant than lymphocytes (34,41). This is supported by a recent report (42) demonstrating that although resident PC T cells exhibit a phenotype indicative of activation, they are suppressed by resident peritoneal Mfs, which outnumber T cells and suppress via an IFN-g and iNOS-dependent mechanism.…”

Section: Discussionmentioning

confidence: 79%

TLR Agonists That Induce IFN-β Abrogate Resident Macrophage Suppression of T Cells

Hamilton

Antignano

Rossum

et al. 2010

The Journal of Immunology

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Section: Discussionmentioning

confidence: 79%

TLR Agonists That Induce IFN-β Abrogate Resident Macrophage Suppression of T Cells

Hamilton

Antignano

Rossum

et al. 2010

The Journal of Immunology

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“…[15][16][17] These works suggested that B lymphocytes are unlikely to play a significant role in the regulation of wound healing. Throughout the course of our studies, we never observed significant numbers of B cells in wounded areas (Fig.…”

Section: Discussionmentioning

confidence: 99%

Antibodies to wounded tissue enhance cutaneous wound healing

et al. 2009

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SummaryThe wound repair process is a highly ordered sequence of events that encompasses haemostasis, inflammatory cell infiltration, tissue regrowth and remodelling. Wound healing follows tissue destruction so we hypothesized that antibodies might bind to wounded tissues, which would facilitate the engulfment of damaged tissues by macrophages. Here, we show that B cells, which produce antibodies to damaged tissues, are engaged in the process of wound healing. Splenectomy delayed wound healing, and transfer of spleen cells into splenectomized mice recovered the delay in wound healing. Furthermore, wound healing in splenectomized nude mice was also delayed. Transfer of enriched B220 + cells by magnetic beads accelerated wound healing in splenectomized mice. We detected immunoglobulin G1 (IgG1) binding to wounded tissues by using fluorescein isothiocyanate-labelled anti-IgG1 6-24 hr after wounding. Splenectomy reduced the amount of IgG1 binding to wounded tissues. Immunoblotting studies revealed several bands, which were reduced by splenectomy. Using immunoprecipitation with anti-IgG bound to protein G we found that the intensity of several bands was lower in the serum from splenectomized mice than in that from sham-operated mice. These bands were matched to myosin IIA, carbamoyl-phosphate synthase, argininosuccinate synthase, actin and a-actinin-4 by liquid chromatography tandem mass spectrometry analysis.

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“…Although the physiological roles of this cytokine remain largely unknown, OSM has been shown to exert a variety of effects on different types of cells. Studies have shown that fibroblasts are target cells for OSM (23,24,36,37) and that T-lymphocyte and monocyte/macrophage infiltration is observed in normal dermal repair as well as fibrotic lesions (38,39). Therefore, OSM could play a role in dermal fibrotic repair or fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Oncostatin M Stimulates the Growth of Dermal Fibroblasts Via a Mitogen-Activated Protein Kinase-Dependent Pathway

Ihn

Tamaki

2000

The Journal of Immunology

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Oncostatin M (OSM), a member of the hemopoietic cytokine family, has been implicated in the process of fibrosis and dermal wound healing. As a part of an ongoing study of the mechanisms of fibrosis and dermal wound healing, we have investigated the mechanism of the growth regulation of dermal fibroblasts by OSM. OSM stimulates the mitogenesis of dermal fibroblasts in a dose-dependent manner. This effect was completely blocked by anti-OSM IgG, but not by anti-IL-6 IgG. Furthermore, OSM induction was abolished by genistein, a tyrosine kinase inhibitor, or by PD98059, a specific mitogen-activated protein (MAP) kinase pathway inhibitor, but not by calphostin C, a protein kinase C inhibitor. Immunoblotting analysis using a specific Ab against phosphorylated MAP kinase (Thr202/Tyr204) showed that OSM induces phosphorylation of MAP kinase in dermal fibroblasts. Furthermore, transient transfection of the dominant-negative mutant MAP kinase into dermal fibroblasts abolished the OSM induction. These results strongly suggest that OSM stimulates the growth of dermal fibroblasts via a MAP kinase-dependent pathway.

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The role of lymphocytes in wound healing

Cited by 98 publications

References 5 publications

TLR Agonists That Induce IFN-β Abrogate Resident Macrophage Suppression of T Cells

TLR Agonists That Induce IFN-β Abrogate Resident Macrophage Suppression of T Cells

Antibodies to wounded tissue enhance cutaneous wound healing

Oncostatin M Stimulates the Growth of Dermal Fibroblasts Via a Mitogen-Activated Protein Kinase-Dependent Pathway

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