We are analyzing https://link.springer.com/article/10.1007/s12026-007-8014-9.

Title:
Th17 cells: a new fate for differentiating helper T cells | Immunologic Research
Description:
Classically naïve CD4+ have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-γ. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-γ was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFβ-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORγt). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFβ-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.
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Keywords {🔍}

google, scholar, article, cas, cells, immunol, interleukin, helper, cell, med, nat, pubmed, inflammation, differentiation, exp, chen, expression, human, cytokine, autoimmune, immunity, development, regulatory, nature, arthritis, production, factor, growth, mckenzie, lineage, stat, inflammatory, producing, oshea, autoimmunity, retinoic, receptor, role, regulates, murphy, research, induce, transforming, laurence, distinct, flavell, induction, dendritic, biol, foxp,

Topics {✒️}

il-17-secreting t-helper phenotype month download article/chapter transforming growth factor-beta interferon-gamma-producing th1 subset cells induce cd4+cd25-foxp3 lamina propria macrophages coenen-de roo cj type ii collagen-stimulated cxc chemokine lix/cxcl5 noncanonical octamer-binding site disrupted ifn-gamma gene cell-mediated intestinal inflammation il-12p40-deficient mice cyclosporin a-sensitive mechanism peripheral cd4+cd25-naive cell-dependent experimental colitis transcription factor foxp3 cytokine receptor subunit bordetella pertussis full article pdf tgf-beta inhibits murine dendritic cells il-23-il-17 immune pathway privacy choices/manage cookies induces autoimmune inflammation anti-interleukin-12 antibody t-bet de waal malefyt de sauvage fj helicobacter hepaticus-induced related subjects central nervous system tumour necrosis factor induce th1 polarization cd4+cd25+ regulatory ivanov ii collagen-induced arthritis herpesvirus saimiri gene lung cxc chemokine exogenous tgf-beta cell-mediated colitis cell-dependent colitis foxp3-expressing regulatory gene-microarray analysis card9-dependent coupling reg cell growth cell differentiation mediated van den bersselaar ifn-gamma regulates inflammatory bowel disease

Schema {🗺️}

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         headline:Th17 cells: a new fate for differentiating helper T cells
         description:Classically naïve CD4+ have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-γ. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-γ was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFβ-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORγt). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFβ-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.
         datePublished:2008-01-03T00:00:00Z
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      headline:Th17 cells: a new fate for differentiating helper T cells
      description:Classically naïve CD4+ have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-γ. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-γ was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFβ-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORγt). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFβ-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.
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         Cytokines
         Interleukins
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         Th1
         Th2
         Th17
         Regulatory T cells
         Immunology
         Allergology
         Medicine/Public Health
         general
         Internal Medicine
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