The role of interleukin 16 in the pathogenesis of selected skin diseases

Purzycka-Bohdan, Dorota; Nedoszytko, Bogusław; Żmijewski, Michał A.; Szczerkowska-Dobosz, Aneta; Zabłotna, Monika; Nowicki, Roman

doi:10.5114/dr.2014.41074

Cited by 2 publications

(2 citation statements)

References 41 publications

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“…and adiponectin was also reduced in infected TCR -/mice vs. infected WT mice. IL-16 typically increases inflammation in the skin and inhibits the wound healing response [90], but adiponectin promotes wound healing by increasing KC proliferation and migration [91]. Therefore, deficits in  T cells may partially account for the previously described defect in sterile wound healing [32,44] via reduced expression of adiponectin.…”

Section: Discussionmentioning

confidence: 99%

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

Reider

Lin

Krouse

et al. 2020

Preprint

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Infection at peripheral sites, such as the skin, activates local innate immune defenses tasked with limiting spread of the pathogen while preserving tissue integrity. T cells bearing γδ T Cell Receptors (TCR), which comprise multiple phenotypically distinct subtypes of cells, reside in normal skin, where they shape immunity to cutaneous infection, prior to onset of an adaptive immune response by conventional αβ CD4+ (TCD4+) and CD8+ (TCD8+) T cells. The mechanisms used by γδ T cells to control virus replication and tissue pathology following cutaneous infection are unknown, so we examined the role of γδ T cells in the response to cutaneous infection with vaccinia virus (VACV). Resident γδ T cells in the skin expanded and combined with recruited γδ T cells to control the pathology observed after cutaneous VACV infection. However, we observed no defect in control of local virus replication or increased systemic spread in mice lacking γδ T cells, despite induction of a cytolytic response in a specialized subset of resident γδ T cells. While examining γδ T cell-mediated control of tissue pathology following cutaneous VACV infection, we identified a unique wound healing signature associated with cutaneous virus infection that has features that are common to, but also features that antagonize, the sterile cutaneous wound healing response. Typically, tissue repair is thought to occur only after clearance of a pathogen, but the viral wound healing signature was evident prior to the peak of virus replication in the skin. Resident and recruited γδ T cells contributed to this wound healing signature through induction of multiple cytokines and growth factors required for efficient wound closure. Therefore, γδ T cells are early mediators of the wound healing response following cutaneous virus infection and are likely important in maintenance of skin barrier function and prevention of secondary bacterial infection.Author Summaryγδ T cells resident in the skin are among the first immune cell types positioned to be able to respond to a virus infection of the skin. Therefore, it was assumed that these cells in the skin play a role similar to their role after widespread infection throughout the body, namely to kill virus infected cells and slow virus replication and spread. However, we found no role for γδ T cells in control of virus replication after infection of the skin. Rather, the γδ T cells functioned as a critical component of a previously unrecognized wound healing response that is started early after virus infection of the skin, and occurs at the same time as the immune response that aims to clear the virus. This study is the first to describe both the early wound healing response after virus infection, and the role of γδ T cells in that response, and this information could allow manipulation of this response to decrease secondary bacterial infection and change scarring after virus skin infections.

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Section: Discussionmentioning

confidence: 99%

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

Reider

Lin

Krouse

et al. 2020

Preprint

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“…In psoriasis patients there is an altered balance of regulatory T cells (Tregs) and Th17 cells [40][41][42][43]. Tregs are lymphocytes that regulate the immune system and suppress the immune response [40], thus preventing development of autoimmune disease. Tregs inhibit the activity of CD4+ and CD8+ T cells leading to decreased production of pro-inflammatory cytokines [28].…”

Section: Th17 Signaling Pathwaymentioning

confidence: 99%

Genetic and Epigenetic Mechanisms of Psoriasis

Arrom

Puig

2023

Genes

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Psoriasis is a disease involving the innate and adaptative components of the immune system, and it is triggered by environmental factors in genetically susceptible individuals. However, its physiopathology is not fully understood yet. Recent technological advances, especially in genome and epigenome-wide studies, have provided a better understanding of the genetic and epigenetic mechanisms to determine the physiopathology of psoriasis and facilitate the development of new drugs. This review intends to summarize the current evidence on genetic and epigenetic mechanisms of psoriasis.

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The role of interleukin 16 in the pathogenesis of selected skin diseases

Cited by 2 publications

References 41 publications

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

γδ T cells mediate a requisite portion of a wound healing response triggered by cutaneous poxvirus infection

Genetic and Epigenetic Mechanisms of Psoriasis

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