Human papilloma virus‐16‐specificCD8+ T‐cell expansions characterize different clinical forms of lichen planus and not lichen sclerosus et atrophicus

Author:

Viguier Manuelle1ORCID,Pérals Corine2ORCID,Poirier Béatrice3,Battistella Maxime4ORCID,Aubin François5ORCID,Bachelez Hervé67ORCID,Prétet Jean‐Luc8ORCID,Gheit Tarik9ORCID,Tommasino Massimo910ORCID,Touzé Antoine11ORCID,Gougeon Marie‐Lise3ORCID,Fazilleau Nicolas2ORCID

Affiliation:

1. Department of dermatology, Hôpital Robert‐Debré University of Reims Champagne‐Ardenne (URCA), EA7509 IRMAIC Reims France

2. Institut Toulousain des Maladies Infectieuses et Inflammatoires (Infinity), CNRS U5051, INSERM U1291 University Toulouse III Toulouse France

3. Institut Pasteur Paris France

4. Sorbonne Paris Cité, Service d'Anatomo‐Pathologie, Hôpital Saint‐Louis Paris France

5. Service de Dermatologie, Centre Hospitalo‐Universitaire (CHU) de Besançon Université de Franche Comté Besançon France

6. Laboratory of Genetics of Skin Diseases, Imagine Institute for Human Genetic Diseases, INSERM U1163 Université de Paris Paris France

7. Department of Dermatology APHP Hôpital Saint‐Louis Paris France

8. Centre National de Référence Papillomavirus, Laboratoire de Biologie Cellulaire et Moléculaire, CHU de Besançon Université Bourgogne Franche Comté Besançon France

9. IARC Lyon France

10. IRCCS Istituto Tumori Giovanni Paolo II Bari Italy

11. UMR INRAE ISP, Université de Tours Tours France

Abstract

AbstractLichen planus (LP) is a cutaneomucosal chronic inflammatory disease characterized by a CD8+cytotoxic T‐lymphocytes (CTL) infiltrate. In erosive oral LP, we found HPV16‐specific activated CTL in lesions, supporting a pathogenic contribution of HPV16. Here, we investigated whether a similar scenario occurs in other clinical forms of LP and in lichen sclerosus et atrophicus (LSA), another chronic disease also affecting the mucosa and/or the skin. Blood CTL from LP and LSA patients expressed significant higher levels of granzyme B, perforin and CD107a proteins than healthy donors. Expansions of TCRVß3+CTL, with presence of TCR clonotypes identical to those previously detected in erosive oral LP, were found both in blood and mucosal/skin lesions of LP, and not of LSA patients. These expansions were enriched with HPV16‐specific CD8+T‐cells as shown by their recognition of the E711‐20immunodominant epitope. In LSA patients, the peripheral repertoire of CTL was oligoclonal for TCRVß6+CTL. Finally, although patients with LP and LSA have developed antibodies against HPV16 capsid L1, antibodies against HPV16 E6 were only observed in patients with LP. Overall, our data collectively suggest an involvement of HPV16‐specific CTL in different clinical forms of LP, not only in erosive oral LP, while a different scenario operates in LSA.

Funder

European Regional Development Fund

Institut National de la Santé et de la Recherche Médicale

Société Française de Dermatologie et de Pathologie Sexuellement Transmissible

Publisher

Wiley

Subject

Dermatology,Molecular Biology,Biochemistry

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