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Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ
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Oxidative stress drives CD8+ T-cell skin trafficking in patients with vitiligo through CXCL16 upregulation by

Shuli Li1, Guannan Zhu1, Yuqi Yang1

  • 1Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Shaanxi, China.

The Journal of Allergy and Clinical Immunology
|November 10, 2016
PubMed
Summary

Oxidative stress in vitiligo increases CXCL16 in keratinocytes, driving CD8+ T-cell skin migration via the CXCL16-CXCR6 pathway. This occurs through unfolded protein response activation, contributing to melanocyte loss.

Keywords:
CD8(+) T cellsCXCL16CXCR6Oxidative stressskin migrationunfolded protein response

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Area of Science:

  • Dermatology
  • Immunology
  • Cell Biology

Background:

  • Vitiligo is associated with increased reactive oxygen species (ROS), impacting melanocytes.
  • The role of ROS in other skin cells like keratinocytes and subsequent immune responses in vitiligo is less understood.
  • CXCL16, expressed by keratinocytes, is implicated in CD8+ T-cell homing to human skin.

Purpose of the Study:

  • To investigate the impact of oxidative stress on human keratinocytes.
  • To determine if oxidative stress influences CD8+ T-cell trafficking via CXCL16 regulation.

Main Methods:

  • Assessed T-cell chemokines and ROS in vitiligo patient serum and lesions.
  • Quantified chemokine production in H2O2-exposed keratinocytes using qPCR and ELISA.
  • Analyzed mediators via qPCR, Western blotting, ELISA, and immunofluorescence.
  • Evaluated CD8+ T-cell migration using transwell assays.

Main Results:

  • Elevated CXCL16 expression correlated with oxidative stress in vitiligo patients.
  • H2O2-induced CXCL16 production resulted from unfolded protein response activation (PKR-eIF2α and IRE1α-XBP1 pathways).
  • Keratinocyte-derived CXCL16 promoted migration of CXCR6+CD8+ T cells from vitiligo patients.
  • CD8+ T-cell infiltration in skin lesions coincided with melanocyte loss.

Conclusions:

  • CXCL16-CXCR6 signaling mediates CD8+ T-cell skin trafficking under oxidative stress in vitiligo.
  • ROS-induced CXCL16 expression in keratinocytes is partly due to unfolded protein response activation.