Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome

By J. Milner, J. Brenchley, A. Laurence, A. Freeman, Brenna J. Hill, K. Elias, Y. Kanno, C. Spalding, H. Elloumi, Michelle L. Paulson and 7 more. Nature, 2008

727 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/31ed9efb3d7b1e3ce5bb3109c5eac6d89312174d

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In Immunology

1. V. Kuchroo
2. T. Korn
3. M. Oukka
4. T. Hirano
5. Robert M. Plenge
6. P. Murray
7. E. Bettelli
8. J. O’Shea

Citations in the corpus

• Differentiation of Effector CD4 T Cell Populations (2010, unknown): “Blood of such patients lacks CD4 T cells capable of producing IL-17, and their purified naive CD4 T cells fail to differentiate into Th17 cells under conditions in which MHC-matched normal cells differentiate quite efficiently (109).”
• Candida albicans—The Virulence Factors and Clinical Manifestations of Infection (2021, background): “, IL-23, IL-21, IL-6) in the differentiation of IL-17 producing T helper cells [116].”
• IL-6 in inflammation, autoimmunity and cancer (2020, background): “Of note is that both STAT3 LOF and STAT1 gain-of-function (GOF) mutations in patients show defects in T h 17 cell differentiation (179, 180).”
• JAK and STAT signaling molecules in immunoregulation and immune-mediated disease. (2012, background): “We now know that STAT3 is critical for Th17 cell differentiation both in mouse and humans, mediating signals by IL-23 and IL-6 (Chen et al., 2006; Milner et al., 2008).”
• Hidden Killers: Human Fungal Infections (2012, unknown): “…as occurs in hyperimmu-noglobulin E syndrome, which results from mutations in the gene ( STAT3 ) that encodes the signal transducer and activator of transcription 3 (STAT3) protein ( 52 ), or in autosomal dominant chronic mucocutaneouscandidiasis,causedbymu-tationsinthe STAT1 gene ( 53 , 54 ) (Fig.”
• Atopic dermatitis (2018, background): “Several studies suggest that nonlesional TEWL in patients with AD is a common end point that is not influenced by FLG status.(44,48,49) However, FLG mutations were associated with higher TEWL in clinically normal forearms in a small cohort of 3-month-old infants in a high-risk cohort; this increase ”