1. Academic Validation
  2. Self-Antigen Presentation by Keratinocytes in the Inflamed Adult Skin Modulates T-Cell Auto-Reactivity

Self-Antigen Presentation by Keratinocytes in the Inflamed Adult Skin Modulates T-Cell Auto-Reactivity

  • J Invest Dermatol. 2015 Aug;135(8):1996-2004. doi: 10.1038/jid.2015.130.
Michael Meister 1 Amel Tounsi 1 Evelyn Gaffal 2 Tobias Bald 2 Maria Papatriantafyllou 1 Julia Ludwig 1 Georg Pougialis 1 Felix Bestvater 3 Luisa Klotz 4 Gerhard Moldenhauer 1 Thomas Tüting 2 Günter J Hämmerling 1 Bernd Arnold 5 Thilo Oelert 1
Affiliations

Affiliations

  • 1 Department of Molecular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • 2 Department of Dermatology and Allergy, Laboratory of Experimental Dermatology, University of Bonn, Bonn, Germany.
  • 3 Core Facility Light Microscopy, German Cancer Research Center (DKFZ), Heidelberg, Germany.
  • 4 Department of Neurology, Clinic for Neurology, University Hospital Münster, Münster, Germany.
  • 5 Department of Molecular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address: b.arnold@dkfz.de.
Abstract

Keratinocytes have a pivotal role in the regulation of immune responses, but the impact of antigen presentation by these cells is still poorly understood, particularly in a situation where the antigen will be presented only in adult life. Here, we generated a transgenic mouse model in which keratinocytes exclusively present a myelin basic protein (MBP) peptide covalently linked to the major histocompatibility complex class II β-chain, solely under inflammatory conditions. In these mice, inflammation caused by epicutaneous contact sensitizer treatment resulted in keratinocyte-mediated expansion of MBP-specific CD4(+) T cells in the skin. Moreover, repeated contact sensitizer application preceding a systemic MBP immunization reduced the reactivity of the respective CD4(+) T cells and lowered the symptoms of the resulting experimental autoimmune encephalomyelitis. This downregulation was CD4(+) T-cell-mediated and dependent on the presence of the immune modulator Dickkopf-3. Thus, presentation of a neo self-antigen by keratinocytes in the inflamed, adult skin can modulate CD4(+) T-cell auto-aggression at a distal organ.

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