Effect of CD4+ and CD8+ cell depletion on wound healing

Davis, Peter A.; Corless, D.; Aspinall, Richard; Wastell, C

doi:10.1046/j.1365-2168.2001.01665.x

Cited by 69 publications

(55 citation statements)

References 15 publications

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“…29 Although several reports examined the role of T cells in wound healing, [30][31][32] the results were contradictory, and there are no papers which examined the T-cell helper function to produce autoantibodies. We did not examine further the (a) Skin samples of 10-week-old C57BL/6 mice were taken by punch biopsy (6 mm) 6 hr after wounding (3 mm).…”

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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Section: Discussionmentioning

confidence: 99%

Antibodies to wounded tissue enhance cutaneous wound healing

et al. 2009

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“…One group reported that CD4 ϩ T-cell depletion did not significantly affect the wound healing in mice, 31 whereas another group showed a significantly impaired wound healing by CD4 ϩ T-cell depletion in rats. 32 On the other hand, the depletion of CD8 ϩ T cells improved wound healing in both groups' studies.…”

Section: Discussionmentioning

confidence: 99%

Inducible Costimulator (ICOS) and ICOS Ligand Signaling Has Pivotal Roles in Skin Wound Healing via Cytokine Production

Maeda

Fujimoto

Matsushita

et al. 2011

The American Journal of Pathology

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“…T lymphocytes have also been studied in wound healing, albeit less extensively. T-cell depletion studies in models of wound healing have produced contradictory results depending on the depletion strategies, species, and mode of injury (64)(65)(66)(67).…”

Section: Discussionmentioning

confidence: 99%

CD11b⁺Ly6G⁻myeloid cells mediate mechanical inflammatory pain hypersensitivity

Ghasemlou

Chiu

Julien

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

157

135

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Pain hypersensitivity at the site of inflammation as a result of chronic immune diseases, pathogenic infection, and tissue injury is a common medical condition. However, the specific contributions of the innate and adaptive immune system to the generation of pain during inflammation have not been systematically elucidated. We therefore set out to characterize the cellular and molecular immune response in two widely used preclinical models of inflammatory pain: (i) intraplantar injection of complete Freund's adjuvant (CFA) as a model of adjuvant-and pathogen-based inflammation and (ii) a plantar incisional wound as a model of tissue injury-based inflammation. Our findings reveal differences in temporal patterns of immune cell recruitment and activation states, cytokine production, and pain in these two models, with CFA causing a nonresolving granulomatous inflammatory response whereas tissue incision induced resolving immune and pain responses. These findings highlight the significant differences and potential clinical relevance of the incisional wound model compared with the CFA model. By using various cell-depletion strategies, we find that, whereas lymphocyte antigen 6 complex locus G (Ly)6G + CD11b + neutrophils and T-cell receptor (TCR) β + T cells do not contribute to the development of thermal or mechanical pain hypersensitivity in either model, proliferating CD11b + Ly6G − myeloid cells were necessary for mechanical hypersensitivity during incisional pain, and, to a lesser extent, CFA-induced inflammation. However, inflammatory (CCR2 + Ly6C hi ) monocytes were not responsible for these effects. The finding that a population of proliferating CD11b + Ly6G − myeloid cells contribute to mechanical inflammatory pain provides a potential cellular target for its treatment in wound inflammation.pain | inflammation | cytokines | monocytes | macrophages

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Effect of CD4+ and CD8+ cell depletion on wound healing

Cited by 69 publications

References 15 publications

Antibodies to wounded tissue enhance cutaneous wound healing

Antibodies to wounded tissue enhance cutaneous wound healing

Inducible Costimulator (ICOS) and ICOS Ligand Signaling Has Pivotal Roles in Skin Wound Healing via Cytokine Production

CD11b⁺Ly6G⁻myeloid cells mediate mechanical inflammatory pain hypersensitivity

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Effect of CD4+ and CD8+ cell depletion on wound healing

Cited by 69 publications

References 15 publications

Antibodies to wounded tissue enhance cutaneous wound healing

Antibodies to wounded tissue enhance cutaneous wound healing

Inducible Costimulator (ICOS) and ICOS Ligand Signaling Has Pivotal Roles in Skin Wound Healing via Cytokine Production

CD11b+Ly6G−myeloid cells mediate mechanical inflammatory pain hypersensitivity

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CD11b⁺Ly6G⁻myeloid cells mediate mechanical inflammatory pain hypersensitivity