IL‐23‐driven encephalo‐tropism and Th17 polarization during CNS‐inflammation in vivo

No abstract is available for this paper.

• Publication year

  2009

• Venue

  European Journal of Immunology

• Publication date

  2009-07-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/eji.200939305PMID 19544494
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17–producing effector T helper cells in vivo

  2009cited by this paper
• IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice.

  2008cited by this paper
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  2008cited by this paper
• IL-23 Promotes Maintenance but Not Commitment to the Th17 Lineage1

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• Interactions among the transcription factors Runx1, RORγt and Foxp3 regulate the differentiation of interleukin 17–producing T cells

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• Cutting Edge: Th1 Cells Facilitate the Entry of Th17 Cells to the Central Nervous System during Experimental Autoimmune Encephalomyelitis1

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• Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation

  2007cited by this paper
• APC-derived cytokines and T cell polarization in autoimmune inflammation.

  2007cited by this paper
• TGF-β and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17 cell–mediated pathology

  2007cited by this paper
• IL-22 Is Expressed by Th17 Cells in an IL-23-Dependent Fashion, but Not Required for the Development of Autoimmune Encephalomyelitis1

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• Faculty Opinions recommendation of TGF-beta and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain T(H)-17 cell-mediated pathology.

  2007cited by this paper
• TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

  2006cited by this paper
• Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

  2006cited by this paper
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• The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.

  2006cited by this paper
• Transforming growth factor-beta induces development of the T(H)17 lineage.

  2006cited by this paper
• Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages

  2005cited by this paper
• IL-23 drives a pathogenic T cell population that induces autoimmune inflammation

  2005cited by this paper
• Dendritic cells permit immune invasion of the CNS in an animal model of multiple sclerosis

  2005cited by this paper
• Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain

  2003cited by this paper
• Role of IL-12 Receptor β1 in Regulation of T Cell Response by APC in Experimental Autoimmune Encephalomyelitis 1

  2003cited by this paper
• Induction of Experimental Autoimmune Encephalomyelitis in IL-12 Receptor-β2-Deficient Mice: IL-12 Responsiveness Is Not Required in the Pathogenesis of Inflammatory Demyelination in the Central Nervous System1

  2003cited by this paper
• Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17*

  2003cited by this paper
• A Receptor for the Heterodimeric Cytokine IL-23 Is Composed of IL-12Rβ1 and a Novel Cytokine Receptor Subunit, IL-23R1

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• Experimental autoimmune encephalitis and inflammation in the absence of interleukin-12.

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  2000cited by this paper
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• The role of Th17 cells in auto-inflammatory neurological disorders.

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• IL-10 Modulates Th17 Pathogenicity during Autoimmune Diseases

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