Recent advances in the IL-17 cytokine family
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TLDR
A review of recent advances in the field of IL-17/IL-17 receptor family biology, with an emphasis on IL- 17A biology.About:
This article is published in Current Opinion in Immunology.The article was published on 2011-10-01 and is currently open access. It has received 258 citations till now. The article focuses on the topics: Janus kinase 1 & Common gamma chain.read more
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Elevated Interleukin‐17A expression in amlodipine‐induced gingival overgrowth
Siddika Selva Sume,Ezel Berker,Yağmur Deniz Ilarslan,Özlem Özer Yücel,Cagman Tan,Samir Goyushov,Sibel Elif Gültekin,Ilhan Tezcan +7 more
TL;DR: Elevated IL-17A expression regardless of inflammation shows that amlodipine might cause an increase of IL- 17A in gingival tissues, which might induce fibrotic changes and EMT inGingival overgrowth tissues.
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Interleukin 17A Derived from γδ T Cell Induces Demyelination of the Brain in Angiostrongylus cantonensis Infection.
TL;DR: In this article, the authors found that blocking IL-17A signalling can attenuate microglia and macrophage activation, thus reducing CNS demyelination and ameliorating the neurobehavioural deficit.
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Interleukin-17 as a spatiotemporal bridge from acute to chronic inflammation: Novel insights from computational modeling.
TL;DR: A systematic review of several acute inflammatory diseases ranging from sepsis and trauma/hemorrhagic shock to the relevant pathology of the decade, COVID-19, points to the cytokine interleukin (IL)-17A as being centrally involved in the propagation of inflammation as discussed by the authors .
Epigenetic modulation of selected immune response genes and altered functions of T lymphocytes and macrophages collectively contribute to autoimmune diabetes protection
TL;DR: In this article, the authors showed that weekly treatment of female prediabetic NOD mice with a low dose of the histone deacetylase inhibitor Trichostatin A (TSA) bestowed long-lasting, irreversible protection against autoimmune diabetes.
References
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The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells.
Ivaylo I. Ivanov,Brent S. McKenzie,Liang Zhou,Carlos E. Tadokoro,Alice Lepelley,Juan J. Lafaille,Daniel J. Cua,Dan R. Littman +7 more
TL;DR: It is shown that the orphan nuclear receptor RORgammat is the key transcription factor that orchestrates the differentiation of this effector cell lineage of proinflammatory T helper cells and its potential as a therapeutic target in inflammatory diseases is highlighted.
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Interleukin 17–producing CD4 + effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
Laurie E. Harrington,Robin D. Hatton,Paul R. Mangan,Henrietta Turner,Theresa L. Murphy,Kenneth M. Murphy,Casey T. Weaver +6 more
TL;DR: 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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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
Heon Park,Zhaoxia Li,Xuexian O. Yang,Seon Hee Chang,Roza Nurieva,Yi Hong Wang,Ying Wang,Leroy Hood,Zhou Zhu,Qiang Tian,Chen Dong +10 more
TL;DR: 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, indicating a unique T helper lineage that regulates tissue inflammation.
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A Genome-Wide Association Study Identifies IL23R as an Inflammatory Bowel Disease Gene
Richard H. Duerr,Kent D. Taylor,Steven R. Brant,Steven R. Brant,John D. Rioux,John D. Rioux,Mark S. Silverberg,Mark J. Daly,Mark J. Daly,A. Hillary Steinhart,Clara Abraham,Miguel Regueiro,Anne M. Griffiths,Themistocles Dassopoulos,Alain Bitton,Huiying Yang,Stephan R. Targan,Lisa W. Datta,Emily O. Kistner,L. Philip Schumm,Annette Lee,Peter K. Gregersen,M. Michael Barmada,Jerome I. Rotter,Dan L. Nicolae,Judy H. Cho +25 more
TL;DR: A highly significant association is found between Crohn's disease and the IL23R gene on chromosome 1p31, which encodes a subunit of the receptor for the proinflammatory cytokine interleukin-23, which prioritize this signaling pathway as a therapeutic target in inflammatory bowel disease.
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
Craig A. Murphy,Claire L. Langrish,Yi Yi Chen,Wendy M. Blumenschein,Terrill K. McClanahan,Robert A. Kastelein,Jonathon D. Sedgwick,Daniel J. Cua +7 more
TL;DR: The data presented here indicate that IL-23 is an essential promoter of end-stage joint autoimmune inflammation, whereas IL-12 paradoxically mediates protection from autoimmune inflammation.