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The antimicrobial peptide LL37 is a T-cell autoantigen in psoriasis

Author

Listed:
  • Roberto Lande

    (Parasitic and Immunomediated Diseases, Istituto Superiore di Sanità
    University Hospital CHUV)

  • Elisabetta Botti

    (Dermatology Unit, Sapienza University of Rome)

  • Camilla Jandus

    (Translational tumor immunology group, Ludwig center for cancer research of the University of Lausanne)

  • Danijel Dojcinovic

    (TC Metrix)

  • Giorgia Fanelli

    (University La Sapienza)

  • Curdin Conrad

    (University Hospital CHUV)

  • Georgios Chamilos

    (University of Texas MD Anderson Cancer Center)

  • Laurence Feldmeyer

    (University Hospital CHUV)

  • Barbara Marinari

    (University Tor Vergata)

  • Susan Chon

    (University of Texas MD Anderson Cancer Center)

  • Luis Vence

    (University of Texas MD Anderson Cancer Center)

  • Valeria Riccieri

    (University La Sapienza)

  • Phillippe Guillaume

    (TC Metrix)

  • Alex A. Navarini

    (University Hospital of Zurich)

  • Pedro Romero

    (TC Metrix)

  • Antonio Costanzo

    (Dermatology Unit, Sapienza University of Rome
    Translational tumor immunology group, Ludwig center for cancer research of the University of Lausanne)

  • Enza Piccolella

    (University La Sapienza)

  • Michel Gilliet

    (University Hospital CHUV)

  • Loredana Frasca

    (Parasitic and Immunomediated Diseases, Istituto Superiore di Sanità
    University Hospital CHUV)

Abstract

Psoriasis is a common T-cell-mediated skin disease with 2–3% prevalence worldwide. Psoriasis is considered to be an autoimmune disease, but the precise nature of the autoantigens triggering T-cell activation remains poorly understood. Here we find that two-thirds of patients with moderate-to-severe plaque psoriasis harbour CD4+ and/or CD8+ T cells specific for LL37, an antimicrobial peptide (AMP) overexpressed in psoriatic skin and reported to trigger activation of innate immune cells. LL37-specific T cells produce IFN-γ, and CD4+ T cells also produce Th17 cytokines. LL37-specific T cells can infiltrate lesional skin and may be tracked in patients blood by tetramers staining. Presence of circulating LL37-specific T cells correlates significantly with disease activity, suggesting a contribution to disease pathogenesis. Thus, we uncover a role of LL37 as a T-cell autoantigen in psoriasis and provide evidence for a role of AMPs in both innate and adaptive immune cell activation.

Suggested Citation

  • Roberto Lande & Elisabetta Botti & Camilla Jandus & Danijel Dojcinovic & Giorgia Fanelli & Curdin Conrad & Georgios Chamilos & Laurence Feldmeyer & Barbara Marinari & Susan Chon & Luis Vence & Valeria, 2014. "The antimicrobial peptide LL37 is a T-cell autoantigen in psoriasis," Nature Communications, Nature, vol. 5(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6621
    DOI: 10.1038/ncomms6621
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    Cited by:

    1. Anissa Fries & Fanny Saidoune & François Kuonen & Isabelle Dupanloup & Nadine Fournier & Ana Cristina Guerra de Souza & Muzlifah Haniffa & Feiyang Ma & Johann E. Gudjonsson & Lennart Roesner & Yang Li, 2023. "Differentiation of IL-26+ TH17 intermediates into IL-17A producers via epithelial crosstalk in psoriasis," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    2. A. Schäbitz & C. Hillig & M. Mubarak & M. Jargosch & A. Farnoud & E. Scala & N. Kurzen & A. C. Pilz & N. Bhalla & J. Thomas & M. Stahle & T. Biedermann & C. B. Schmidt-Weber & F. Theis & N. Garzorz-St, 2022. "Spatial transcriptomics landscape of lesions from non-communicable inflammatory skin diseases," Nature Communications, Nature, vol. 13(1), pages 1-13, December.

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