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Pellino-1 promotes intrinsic activation of skin-resident IL-17A-producing T cells in psoriasis.
Kim, Sung Hee; Oh, Jongwook; Roh, Won Seok; Park, Jeyun; Chung, Kyung Bae; Lee, Gwang Hee; Lee, Youn Sook; Kim, Jong Hoon; Lee, Heung Kyu; Lee, Ho; Park, Chang-Ook; Kim, Do-Young; Lee, Min-Geol; Kim, Tae-Gyun.
Afiliación
  • Kim SH; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  • Oh J; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 FOUR Project for Medical Science, Yonsei University College of Med
  • Roh WS; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  • Park J; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  • Chung KB; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  • Lee GH; Bridge Biotherapeutics Inc, Seongnam-si, Korea.
  • Lee YS; Bridge Biotherapeutics Inc, Seongnam-si, Korea.
  • Kim JH; Deparment of Dermatology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
  • Lee HK; Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Korea.
  • Lee H; Graduate School of Cancer Science and Policy, National Cancer Center, Gyeonggi, Korea.
  • Park CO; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Brain Korea 21 FOUR Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
  • Kim DY; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea.
  • Lee MG; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea. Electronic address: mglee@yuhs.ac.
  • Kim TG; Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Korea; Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Korea. Electronic address: tgmed83@yuhs.ac.
J Allergy Clin Immunol ; 151(5): 1317-1328, 2023 05.
Article en En | MEDLINE | ID: mdl-36646143
BACKGROUND: Psoriasis is a chronically relapsing inflammatory skin disease primarily perpetuated by skin-resident IL-17-producing T (T17) cells. Pellino-1 (Peli1) belongs to a member of E3 ubiquitin ligase mediating immune receptor signaling cascades, including nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) pathway. OBJECTIVE: We explored the potential role of Peli1 in psoriatic inflammation in the context of skin-resident T17 cells. METHODS: We performed single-cell RNA sequencing of relapsing and resolved psoriatic lesions with analysis for validation data set of psoriasis. Mice with systemic and conditional depletion of Peli1 were generated to evaluate the role of Peli1 in imiquimod-induced psoriasiform dermatitis. Pharmacologic inhibition of Peli1 in human CD4+ T cells and ex vivo human skin cultures was also examined to evaluate its potential therapeutic implications. RESULTS: Single-cell RNA sequencing analysis revealed distinct T-cell subsets in relapsing psoriasis exhibiting highly enriched gene signatures for (1) tissue-resident T cells, (2) T17 cells, and (3) NF-κB signaling pathway including PELI1. Peli1-deficient mice were profoundly protected from psoriasiform dermatitis, with reduced IL-17A production and NF-κB activation in γδ T17 cells. Mice with conditional depletion of Peli1 treated with FTY720 revealed that Peli1 was intrinsically required for the skin-resident T17 cell immune responses. Notably, pharmacologic inhibition of Peli1 significantly ameliorated murine psoriasiform dermatitis and IL-17A production from the stimulated human CD4+ T cells and ex vivo skin explants modeling psoriasis. CONCLUSION: Targeting Peli1 would be a promising therapeutic strategy for psoriasis by limiting skin-resident T17 cell immune responses.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Psoriasis / Dermatitis Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: J Allergy Clin Immunol Año: 2023 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Psoriasis / Dermatitis Tipo de estudio: Prognostic_studies Límite: Animals / Humans Idioma: En Revista: J Allergy Clin Immunol Año: 2023 Tipo del documento: Article Pais de publicación: Estados Unidos