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Nat Commun. 2014 Dec 3;5:5621. doi: 10.1038/ncomms6621.

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

Author information

1
1] Department of Infectious, Parasitic and Immunomediated Diseases, Istituto Superiore di Sanità, 00100 Rome, Italy [2] Department of Dermatology, University Hospital CHUV, 1011 Lausanne, Switzerland.
2
Dermatology Unit, NESMOS Department, Sapienza University of Rome, 00100 Rome, Italy.
3
Translational tumor immunology group, Ludwig center for cancer research of the University of Lausanne, Lausanne 1066, Switzerland.
4
TC Metrix, Epalinge 1066, Switzerland.
5
Department of Biology and Biotechnology 'C. Darwin', University La Sapienza, Rome, 00100 Italy.
6
Department of Dermatology, University Hospital CHUV, 1011 Lausanne, Switzerland.
7
Department of Immunology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
8
Department of Dermatology, University Tor Vergata, 00100 Rome, Italy.
9
Department of Dermatology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
10
Department of Melanoma Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
11
Division of Rheumatology, Department of Clinical Medicine and Therapy, University La Sapienza, 00100 Rome, Italy.
12
Department of Dermatology, University Hospital of Zurich, 8091 Zurich, Switzerland.
13
1] Dermatology Unit, NESMOS Department, Sapienza University of Rome, 00100 Rome, Italy [2] Translational tumor immunology group, Ludwig center for cancer research of the University of Lausanne, Lausanne 1066, Switzerland.

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.

PMID:
25470744
DOI:
10.1038/ncomms6621
[Indexed for MEDLINE]

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