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Clinically resolved psoriatic lesions contain psoriasis-specific IL-17-producing αβ T cell clones.

  • Matos, Tiago R1, 2, 3
  • O'Malley, John T1
  • Lowry, Elizabeth L1
  • Hamm, David4
  • Kirsch, Ilan R4
  • Robins, Harlan S4
  • Kupper, Thomas S1
  • Krueger, James G5
  • Clark, Rachael A1
  • 1 Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
  • 2 Instituto de Medicina Molecular, Faculty of Medicine, University of Lisbon, Lisbon, Portugal. , (Portugal)
  • 3 Academic Medical Center, Department of Dermatology, University of Amsterdam, Amsterdam, The Netherlands. , (Netherlands)
  • 4 Adaptive Biotechnologies, Seattle, Washington, USA.
  • 5 Department of Dermatology, Rockefeller University, New York, New York, USA.
Published Article
Journal of Clinical Investigation
American Society for Clinical Investigation
Publication Date
Nov 01, 2017
DOI: 10.1172/JCI93396
PMID: 28945199


In psoriasis, an IL-17-mediated inflammatory skin disease, skin lesions resolve with therapy, but often recur in the same locations when therapy is discontinued. We propose that residual T cell populations in resolved psoriatic lesions represent the pathogenic T cells of origin in this disease. Utilizing high-throughput screening (HTS) of the T cell receptor (TCR) and immunostaining, we found that clinically resolved psoriatic lesions contained oligoclonal populations of T cells that produced IL-17A in both resolved and active psoriatic lesions. Putative pathogenic clones preferentially utilized particular Vβ and Vα subfamilies. We identified 15 TCRβ and 4 TCRα antigen receptor sequences shared between psoriasis patients and not observed in healthy controls or other inflammatory skin conditions. To address the relative roles of αβ versus γδ T cells in psoriasis, we carried out TCR/δ HTS. These studies demonstrated that the majority of T cells in psoriasis and healthy skin are αβ T cells. γδ T cells made up 1% of T cells in active psoriasis, less than 1% in resolved psoriatic lesions, and less than 2% in healthy skin. All of the 70 most frequent putative pathogenic T cell clones were αβ T cells. In summary, IL-17-producing αβ T cell clones with psoriasis-specific antigen receptors exist in clinically resolved psoriatic skin lesions. These cells likely represent the disease-initiating pathogenic T cells in psoriasis, suggesting that lasting control of this disease will require suppression of these resident T cell populations.

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