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Th2 Cells in Health and Disease.
Nakayama, Toshinori; Hirahara, Kiyoshi; Onodera, Atsushi; Endo, Yusuke; Hosokawa, Hiroyuki; Shinoda, Kenta; Tumes, Damon J; Okamoto, Yoshitaka.
Afiliação
  • Nakayama T; Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; email: tnakayama@faculty.chiba-u.jp , hiraharak@chiba-u.jp , a-onodera@faculty.chiba-u.jp , san3tamariayuyu@chiba-u.jp , hiroyuki@caltech.edu , kenta.shinoda@nih.gov , Damon.Tumes@sahmri.com , yokamoto@fa
  • Hirahara K; AMED-CREST, AMED, Chiba 260-8670, Japan.
  • Onodera A; Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; email: tnakayama@faculty.chiba-u.jp , hiraharak@chiba-u.jp , a-onodera@faculty.chiba-u.jp , san3tamariayuyu@chiba-u.jp , hiroyuki@caltech.edu , kenta.shinoda@nih.gov , Damon.Tumes@sahmri.com , yokamoto@fa
  • Endo Y; Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; email: tnakayama@faculty.chiba-u.jp , hiraharak@chiba-u.jp , a-onodera@faculty.chiba-u.jp , san3tamariayuyu@chiba-u.jp , hiroyuki@caltech.edu , kenta.shinoda@nih.gov , Damon.Tumes@sahmri.com , yokamoto@fa
  • Hosokawa H; Institute for Global Prominent Research, Chiba University, Chiba 260-8670, Japan.
  • Shinoda K; Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; email: tnakayama@faculty.chiba-u.jp , hiraharak@chiba-u.jp , a-onodera@faculty.chiba-u.jp , san3tamariayuyu@chiba-u.jp , hiroyuki@caltech.edu , kenta.shinoda@nih.gov , Damon.Tumes@sahmri.com , yokamoto@fa
  • Tumes DJ; Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; email: tnakayama@faculty.chiba-u.jp , hiraharak@chiba-u.jp , a-onodera@faculty.chiba-u.jp , san3tamariayuyu@chiba-u.jp , hiroyuki@caltech.edu , kenta.shinoda@nih.gov , Damon.Tumes@sahmri.com , yokamoto@fa
  • Okamoto Y; Department of Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan; email: tnakayama@faculty.chiba-u.jp , hiraharak@chiba-u.jp , a-onodera@faculty.chiba-u.jp , san3tamariayuyu@chiba-u.jp , hiroyuki@caltech.edu , kenta.shinoda@nih.gov , Damon.Tumes@sahmri.com , yokamoto@fa
Annu Rev Immunol ; 35: 53-84, 2017 04 26.
Article em En | MEDLINE | ID: mdl-27912316
ABSTRACT
Helper T (Th) cell subsets direct immune responses by producing signature cytokines. Th2 cells produce IL-4, IL-5, and IL-13, which are important in humoral immunity and protection from helminth infection and are central to the pathogenesis of many allergic inflammatory diseases. Molecular analysis of Th2 cell differentiation and maintenance of function has led to recent discoveries that have refined our understanding of Th2 cell biology. Epigenetic regulation of Gata3 expression by chromatin remodeling complexes such as Polycomb and Trithorax is crucial for maintaining Th2 cell identity. In the context of allergic diseases, memory-type pathogenic Th2 cells have been identified in both mice and humans. To better understand these disease-driving cell populations, we have developed a model called the pathogenic Th population disease induction model. The concept of defined subsets of pathogenic Th cells may spur new, effective strategies for treating intractable chronic inflammatory disorders.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Células Th2 / Helmintíase / Hipersensibilidade Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Annu Rev Immunol Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Células Th2 / Helmintíase / Hipersensibilidade Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Annu Rev Immunol Ano de publicação: 2017 Tipo de documento: Article