Human papilloma virus‐16‐specific CD8+ T‐cell expansions characterize different clinical forms of lichen planus and not lichen sclerosus et atrophicus

• Published in: Experimental dermatology Vol. 32; no. 6; pp. 859 - 868
• Main Authors: Viguier, Manuelle, Pérals, Corine, Poirier, Béatrice, Battistella, Maxime, Aubin, François, Bachelez, Hervé, Prétet, Jean‐Luc, Gheit, Tarik, Tommasino, Massimo, Touzé, Antoine, Gougeon, Marie‐Lise, Fazilleau, Nicolas
• Format: Journal Article
• Language: English
• Published: Denmark Wiley Subscription Services, Inc 01.06.2023; Wiley
• Subjects: Antibodies; CD8 antigen; CD8-Positive T-Lymphocytes - metabolism; cytotoxic T lymphocytes; Cytotoxicity; Dermatology; Epitopes; Granzyme B; Human health and pathology; human papilloma virus; Human papillomavirus; Human papillomavirus 16; Human Papillomavirus Viruses; Humans; Inflammatory diseases; Lichen planus; Lichen Planus - pathology; Lichen Planus, Oral; Lichen Sclerosus et Atrophicus - metabolism; Lichen Sclerosus et Atrophicus - pathology; Life Sciences; Lymphocytes; Lymphocytes T; Perforin; Skin diseases; Skin lesions; T‐cell; T‐cell receptor; T-cell receptor; cytotoxic T lymphocytes; human papilloma virus; T-cell; lichen planus
• ISSN: 0906-6705; 1600-0625
• DOI: 10.1111/exd.14788

Lichen 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 E711‐20 immunodominant 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.