HSP70i is a critical component of the immune response leading to vitiligo

Jeffrey A. Mosenson, Andrew Zloza, Jared Klarquist, Allison J. Barfuss, Jose A. Guevara-Patino, I. Caroline Le Poole*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


HSP70i and other stress proteins have been used in anti-tumor vaccines. This begs the question whether HSP70i plays a unique role in immune activation. We vaccinated inducible HSP70i (Hsp70-1) knockout mice and wild-type animals with optimized TRP-1, a highly immunogenic melanosomal target molecule. We were unable to induce robust and lasting depigmentation in the Hsp70-1 knockout mice, and in vivo cytolytic assays revealed a lack of cytotoxic T-lymphocyte activity. Absence of T-cell infiltration to the skin and maintenance of hair follicle melanocytes were observed. By contrast, depigmentation proceeded without interruption in mice lacking a tissue-specific constitutive isoform of HSP70 (Hsp70-2) vaccinated with TRP-2. Next, we demonstrated that HSP70i was necessary and sufficient to accelerate depigmentation in vitiligo-prone Pmel-1 mice, accompanied by lasting phenotypic changes in dendritic cell subpopulations. In summary, these studies assign a unique function to HSP70i in vitiligo and identify HSP70i as a targetable entity for treatment.

Original languageEnglish (US)
Pages (from-to)88-98
Number of pages11
JournalPigment Cell and Melanoma Research
Issue number1
StatePublished - Jan 2012


  • Autoimmunity
  • HSP70
  • Knockout mouse
  • Vitiligo

ASJC Scopus subject areas

  • Oncology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Dermatology


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