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Gamma delta t cells are reduced and rendered unresponsive by hyperglycemia and chronic tnf alpha in mouse models of obesity and metabolic disease

Academic Article
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Overview

authors

  • Taylor, K. R.
  • Mills, R. E.
  • Costanzo, A. E.
  • Jameson, Julie

publication date

  • July 2010

journal

  • PLoS One  Journal

abstract

  • Epithelial cells provide an initial line of defense against damage and pathogens in barrier tissues such as the skin; however this balance is disrupted in obesity and metabolic disease. Skin gammadelta T cells recognize epithelial damage, and release cytokines and growth factors that facilitate wound repair. We report here that hyperglycemia results in impaired skin gammadelta T cell proliferation due to altered STAT5 signaling, ultimately resulting in half the number of gammadelta T cells populating the epidermis. Skin gammadelta T cells that overcome this hyperglycemic state are unresponsive to epithelial cell damage due to chronic inflammatory mediators, including TNFalpha. Cytokine and growth factor production at the site of tissue damage was partially restored by administering neutralizing TNFalpha antibodies in vivo. Thus, metabolic disease negatively impacts homeostasis and functionality of skin gammadelta T cells, rendering host defense mechanisms vulnerable to injury and infection.

subject areas

  • Animals
  • Antibodies
  • Cell Line
  • Cell Proliferation
  • Cells, Cultured
  • Disease Models, Animal
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Hyperglycemia
  • In Vitro Techniques
  • Metabolic Diseases
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Obesity
  • Oligonucleotide Array Sequence Analysis
  • Phosphorylation
  • Polymerase Chain Reaction
  • STAT5 Transcription Factor
  • Tumor Necrosis Factor-alpha
  • Wound Healing
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Identity

PubMed Central ID

  • PMC2896399

International Standard Serial Number (ISSN)

  • 1932-6203

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0011422

PubMed ID

  • 20625397
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Additional Document Info

start page

  • e11422

volume

  • 5

issue

  • 7

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