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We began analyzing https://www.nature.com/articles/ni1254, but it redirected us to https://www.nature.com/articles/ni1254. The analysis below is for the second page.

Title[redir]:
Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages | Nature Immunology
Description:
CD4+ T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (TH1) or TH2 lineages and instead favor the idea of a distinct effector lineage we call

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


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While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Doi.org could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

article, cas, google, scholar, cells, nature, immunol, murphy, cell, interleukin, autoimmune, immunity, development, stat, tbet, access, mice, cytokine, content, immunology, helper, ifnγ, lineage, distinct, exp, med, inflammation, cookies, naive, nat, expression, science, privacy, data, effector, type, role, rev, responses, differentiation, production, encephalomyelitis, induction, receptor, information, producing, weaver, interferonγ, signaling, critical,

Topics {✒️}

nature portfolio permissions reprints privacy policy th17 cell-derived tgf-β1 advertising social media nature 421 nature author information authors jak-stat signaling pathway tlr-activated dendritic cells author correspondence proximal ifn-gamma promoter t-helper 1 development–resolved silencing t-bet defines disrupted interferon-γ genes disrupted ifn-γ gene delayed-type hypersensitivity responses cd4+cd8+tcrlo thymocytes data protection promote ifn-γ production springerlink instant access permissions il-12p35-deficient mice counting antigen-specific cd8 personal data rocaglamide promotes infiltration il-4-independent mechanism joint autoimmune inflammation th1 development mediated present data experimental autoimmune encephalomyelitis induces autoimmune inflammation enhanced th1 development th17 cell heterogeneity biological activities similar privacy transcription factor gata-3 il-26+ th17 intermediates competing financial interests il-17-producing cells shared developmental pathway issue learn il-12-dependent selection ifn-γ plays ifn-α signal ifn-γ production interleukin-23 promotes independent mechanisms european economic area

Schema {🗺️}

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         headline:Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
         description:CD4+ T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (TH1) or TH2 lineages and instead favor the idea of a distinct effector lineage we call 'TH-17'. The development of TH-17 cells from naive precursor cells was potently inhibited by interferon-γ (IFN-γ) and IL-4, whereas committed TH-17 cells were resistant to suppression by TH1 or TH2 cytokines. In the absence of IFN-γ and IL-4, IL-23 induced naive precursor cells to differentiate into TH-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
         datePublished:2005-10-02T00:00:00Z
         dateModified:2005-10-02T00:00:00Z
         pageStart:1123
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      headline:Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
      description:CD4+ T cells producing interleukin 17 (IL-17) are associated with autoimmunity, although the precise mechanisms that control their development are undefined. Here we present data that challenge the idea of a shared developmental pathway with T helper type 1 (TH1) or TH2 lineages and instead favor the idea of a distinct effector lineage we call 'TH-17'. The development of TH-17 cells from naive precursor cells was potently inhibited by interferon-γ (IFN-γ) and IL-4, whereas committed TH-17 cells were resistant to suppression by TH1 or TH2 cytokines. In the absence of IFN-γ and IL-4, IL-23 induced naive precursor cells to differentiate into TH-17 cells independently of the transcription factors STAT1, T-bet, STAT4 and STAT6. These findings provide a basis for understanding how inhibition of IFN-γ signaling enhances development of pathogenic TH-17 effector cells that can exacerbate autoimmunity.
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