STAT3 mutations in the hyper-IgE syndrome.

By S. Holland, F. DeLeo, H. Elloumi, A. Hsu, G. Uzel, N. Brodsky, A. Freeman, A. Demidowich, Joie N. Davis, M. Turner and 15 more. New England Journal of Medicine, 2007

1,182 citations recorded by the source corpus.

Subfields: Emergency Medical Services, Immunology

View Paper: https://www.semanticscholar.org/paper/c1d2bbab355088e1570dc5a942519f6b8ea31124

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. J. O’Shea
2. D. Artis
3. Y. Kanno
4. A. Laurence
5. P. Murray
6. F. Powrie
7. Huiyuan Zhang
8. S. Watowich

Citations in the corpus

• Differentiation of Effector CD4 T Cell Populations (2010, neutral): “STAT3—STAT3 is activated by IL-6, IL-21, and IL-23, cytokines that are involved in Th17 cell differentiation, amplification, and maintenance (21–24, 41, 42).”
• STAT3 signaling in immunity (2016, background): “Elevated basal and TLR4-responsive expression of pro-inflammatory cytokines was found in peripheral blood neutrophils and mononuclear cells from individuals with STAT3 AD-HIES [63], suggesting human STAT3 restrains pro-inflammatory gene expression.”
• Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis (2010, background): “Patients with Job’s or Hyper IgE Syndrome (HIES) have dominant-negative mutations of STAT3 and are deficient in Th17 cells, underscoring the close link between STAT3 and Th17 cells (Holland et al., 2007; Ma et al., 2008; Milner et al., 2008; Minegishi et al., 2007).”
• Border patrol: regulation of immunity, inflammation and tissue homeostasis at barrier surfaces by IL-22 (2011, background): “Consistent with the role of IL-22 in promoting immunity to fungal and bacterial pathogens at barrier surfaces in mouse models, patients with this syndrome also suffer severe and recurrent secondary infections in the skin, lung and intestin”
• The JAK-STAT Pathway: Impact on Human Disease and Therapeutic Intervention (2015, background): “Underlying many cases of autosomal dominant HIES are dominant negative mutations of STAT3 (5, 6).”
• Cytokine signaling modules in inflammatory responses. (2008, background): “…leukocytes isolated from humans bearing mutations in STAT3 and suffering from Job’s syndrome, are characterized the overproduction cytokines and chemokines following stimulation with TLR agonists, bacteria and interferons (Holland et al., 2007; Minegishi et al., 2007; Milner et al., 2008).”
• Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease (2012, neutral): “(DK062429-S1 and Crohn’s & Colitis Foundation of America, Senior Investigator Award (5-2229)) and R.”