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IL-17+ CD8+ T cells: Differentiation, phenotype and role in inflammatory disease.
Srenathan, Ushani; Steel, Kathryn; Taams, Leonie S.
Afiliação
  • Srenathan U; Centre for Molecular and Cellular Biology of Inflammation, Division of Immunology, Infection & Inflammatory Disease, King's College London, London, UK.
  • Steel K; Centre for Molecular and Cellular Biology of Inflammation, Division of Immunology, Infection & Inflammatory Disease, King's College London, London, UK.
  • Taams LS; Centre for Molecular and Cellular Biology of Inflammation, Division of Immunology, Infection & Inflammatory Disease, King's College London, London, UK. Electronic address: leonie.taams@kcl.ac.uk.
Immunol Lett ; 178: 20-6, 2016 10.
Article em En | MEDLINE | ID: mdl-27173097
ABSTRACT
The pro-inflammatory cytokine interleukin-17A (IL-17) has been the subject of research by many groups worldwide. IL-17 expression is often associated with a specific subset of CD4+ T cells (the so-called Th17 cells); however various other immune cell subsets can also synthesise and express IL-17, including CD8+ T cells. Here we review recent data regarding the presence of IL-17+ CD8+ T cells (also known as Tc17 cells) in human inflammatory disease, discuss current knowledge regarding the culture conditions required for the differentiation of these cells in humans and mice, and describe key phenotypic and functional features. Collectively, this information may shed light on the potential pathogenic role that IL-17+ CD8+ T cells may play in human inflammatory disease.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Subpopulações de Linfócitos T / Linfócitos T CD8-Positivos / Interleucina-17 Tipo de estudo: Etiology_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Subpopulações de Linfócitos T / Linfócitos T CD8-Positivos / Interleucina-17 Tipo de estudo: Etiology_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article