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We began analyzing https://www.nature.com/articles/ni1261, but it redirected us to https://www.nature.com/articles/ni1261. The analysis below is for the second page.

Title[redir]:
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17 | Nature Immunology
Description:
Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-Ξ³ negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.

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πŸ™οΈ Massive Traffic: 50M - 100M visitors per month


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Keywords {πŸ”}

article, pubmed, google, scholar, cas, nature, interleukin, cells, cell, immunol, inflammation, access, immunology, content, dong, autoimmune, helper, production, family, immune, immunity, med, cookies, yang, expression, glimcher, central, factor, privacy, data, distinct, lineage, regulates, wang, type, cytokine, exp, mice, function, information, tissue, park, chen, differentiation, effector, chemokine, pdf, open, rev, responses,

Topics {βœ’οΈ}

nature portfolio cancer research institute permissions reprints privacy policy advertising th1 development social media nature 421 nature 409 nature tumor necrosis factor-Ξ± proto-oncogene c-maf author correspondence interferon-Ξ³ negatively regulated t-bet-deficient mice human b7–h3 genes sputum metalloproteinase-9/tissue inhibitor il-17a expressing cd4+ permissions springerlink instant access experimental autoimmune encephalomyelitis cd4+ t-cell subsets data protection yi-hong wang personal data microarray data chen dong lung cxc chemokine rocaglamide promotes infiltration privacy transcription factor gata-3 interleukin-17 family members regulates tissue inflammation maf-transgenic mice competing financial interests article park sputum matrix metalloproteinase-9 induces autoimmune inflammation leroy hood issue learn interferon-Ξ³ production tissue-specific expression transcription factors required explore content subscription content joint autoimmune inflammation european economic area seon hee chang costimulatory molecules cd28 institutional subscriptions read

Schema {πŸ—ΊοΈ}

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         description:Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-γ negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.
         datePublished:2005-10-02T00:00:00Z
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      headline:A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
      description:Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-γ negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.
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Social Networks {πŸ‘}(1)

External Links {πŸ”—}(270)

Analytics and Tracking {πŸ“Š}

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Libraries {πŸ“š}

  • Prism.js
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Emails and Hosting {βœ‰οΈ}

Mail Servers:

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Name Servers:

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CDN Services {πŸ“¦}

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