Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

Dysfunctional gamma delta t cells contribute to impaired keratinocyte homeostasis in mouse models of obesity

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

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

publication date

  • December 2011

journal

  • Journal of Investigative Dermatology  Journal

abstract

  • Skin complications and chronic non-healing wounds are common in obesity, metabolic disease, and type 2 diabetes. Epidermal γδ T cells normally produce keratinocyte growth factors, participate in wound repair, and are necessary for keratinocyte homeostasis. We have determined that in γδ T cell-deficient mice, there are reduced numbers of keratinocytes and the epidermis exhibits a flattened, thinner structure with fewer basal keratinocytes. This is important in obesity, where skin-resident γδ T cells are reduced and rendered dysfunctional. Similar to γδ T cell-deficient mice, keratinocytes are reduced and the epidermal structure is altered in two obese mouse models. Even in regions where γδ T cells are present, there are fewer keratinocytes in obese mice, indicating that dysfunctional γδ T cells are unable to regulate keratinocyte homeostasis. The impact of absent or impaired γδ T cells on epidermal structure is exacerbated in obesity as E-cadherin localization and expression are additionally altered. These studies reveal that γδ T cells are unable to regulate keratinocyte homeostasis in obesity and that the obese environment further impairs skin structure by altering cell-cell adhesion. Together, impaired keratinocyte homeostasis and epidermal barrier function through direct and indirect mechanisms result in susceptibility to skin complications, chronic wounds, and infection.

subject areas

  • Animals
  • Cadherins
  • Diabetes Mellitus, Type 2
  • Disease Models, Animal
  • Female
  • Homeostasis
  • Keratinocytes
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Obesity
  • Receptors, Antigen, T-Cell, gamma-delta
  • T-Lymphocyte Subsets
scroll to property group menus

Identity

PubMed Central ID

  • PMC3213272

International Standard Serial Number (ISSN)

  • 0022-202X

Digital Object Identifier (DOI)

  • 10.1038/jid.2011.241

PubMed ID

  • 21833015
scroll to property group menus

Additional Document Info

start page

  • 2409

end page

  • 2418

volume

  • 131

issue

  • 12

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support