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Interleukin-27 priming of T cells controls IL-17 production in trans via induction of the ligand PD-L1.
Hirahara, Kiyoshi; Ghoreschi, Kamran; Yang, Xiang-Ping; Takahashi, Hayato; Laurence, Arian; Vahedi, Golnaz; Sciumè, Giuseppe; Hall, Aisling O'Hara; Dupont, Christopher D; Francisco, Loise M; Chen, Qian; Tanaka, Masao; Kanno, Yuka; Sun, Hong-Wei; Sharpe, Arlene H; Hunter, Christopher A; O'Shea, John J.
Afiliação
  • Hirahara K; Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA. hiraharak@mail.nih.gov
Immunity ; 36(6): 1017-30, 2012 Jun 29.
Article em En | MEDLINE | ID: mdl-22726954
Interleukin-27 (IL-27) is a key immunosuppressive cytokine that counters T helper 17 (Th17) cell-mediated pathology. To identify mechanisms by which IL-27 might exert its immunosuppressive effect, we analyzed genes in T cells rapidly induced by IL-27. We found that IL-27 priming of naive T cells upregulated expression of programmed death ligand 1 (PD-L1) in a signal transducer and activator of transcription 1 (STAT1)-dependent manner. When cocultured with naive CD4(+) T cells, IL-27-primed T cells inhibited the differentiation of Th17 cells in trans through a PD-1-PD-L1 interaction. In vivo, coadministration of naive TCR transgenic T cells (2D2 T cells) with IL-27-primed T cells expressing PD-L1 inhibited the development of Th17 cells and protected from severe autoimmune encephalomyelitis. Thus, these data identify a suppressive activity of IL-27, by which CD4(+) T cells can restrict differentiation of Th17 cells in trans.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interleucinas / Interleucina-17 / Células Th17 / Antígeno B7-H1 Tipo de estudo: Etiology_studies / Prognostic_studies Idioma: En Ano de publicação: 2012 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interleucinas / Interleucina-17 / Células Th17 / Antígeno B7-H1 Tipo de estudo: Etiology_studies / Prognostic_studies Idioma: En Ano de publicação: 2012 Tipo de documento: Article