PMC . NCBI . NLM . NIH . GOV {
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We are analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC4281037/.
Title:
IL-23-IL-17 immune axis: Discovery, Mechanistic Understanding, and Clinical Testing - PMC
Description:
With the discovery of Th17 cells, the past decade has witnessed a major revision of the T helper subset paradigm and significant progress has been made deciphering the molecular mechanisms for T cell lineage commitment and function. In this review, ...
Website Age:
27 years and 8 months (reg. 1997-10-02).
Title:
IL-23-IL-17 immune axis: Discovery, Mechanistic Understanding, and Clinical Testing - PMC
Description:
With the discovery of Th17 cells, the past decade has witnessed a major revision of the T helper subset paradigm and significant progress has been made deciphering the molecular mechanisms for T cell lineage commitment and function. In this review, ...
Website Age:
27 years and 8 months (reg. 1997-10-02).
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🌠 Phenomenal Traffic: 5M - 10M visitors per month
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Keywords {🔍}
doi, cells, google, scholar, pubmed, pmc, article, free, cell, signaling, nature, disease, expression, psoriasis, differentiation, inflammatory, ilr, interleukin, immunology, receptor, immunity, stat, nct, journal, rorγt, transcription, factor, autoimmune, cytokines, patients, phase, inflammation, activation, act, development, crohns, tgfβ, factors, lineage, arthritis, protein, traf, medicine, studies, human, cytokine, genes, immunol, batf, candidiasis,
Topics {✒️}
granulocyte–macrophage colony-stimulating factor transforming growth factor-beta interferon-gamma-expressing th17 cells granulocyte colony-stimulating factor transforming growth factor-β il-17r-knockout mouse models atopic dermatitis compared inherited il-12p40 deficiency il-17r-mediated signaling axis double-blind placebo-controlled trial tumor necrosis factor-alpha erk1/2-dependent nf-kappab mitogen-activated protein kinase ubiquitin-specific protease usp25 il-17-induced nf-κb activation restricts il-23r deficiency ccaat/enhancer-binding protein siderophore-mediated iron acquisition selective nf-kappab activation il-17-induced act1-mediated cxcl1 pre-existent enhancer landscape anti-il-17/il-17ra therapy pmc beta search added anti-inflammatory benefits chip-seq analysis gm-csf-deficient th17 cells hyper-ige syndrome ubiquitin-editing enzyme a20 obligate th17-inducing factor jun n-terminal kinase pro-inflammatory signaling cascades surpassing anti-tnf therapy159 il-17-induced nf-{kappa} anti-il-17 mabs herald genome-wide association study anti-il-17a-treated patients scfbeta-trcp-mediated degradation autosomal dominant-negative mutations anti-il-17ra-treated patients upregulating il-23r expression53 groups evaluated anti-il-17 anti-interleukin-17-receptor antibody naturally-occurring neutralizing antibodies ccaat/enhancer-binding proteins primaly anti-tnf ‘failures il-17-induced antimicrobial protein il-23-il-17 immune axis cell-dependent iga responses dampens il-17-dependent signals116 canonical nf-κb pathway
Questions {❓}
- Do they undergo complete epigenetic remodeling of Th17 associated genes, or do they retain epigenetic evidence of their Th17 origins?
- Master regulators or lineage-specifying?
- Other?
- Staph aureus?
- Reactivity?
- Susceptibility?
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