Evidence map›Paper›PMID 26574998›Full record

ReviewCurrent opinion in hematology2016

Signal transducer and activator of transcription 3: a year in review.

Lisa R Forbes, Josh Milner, Elie Haddad

Abstract readReview
In one paragraph

Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 70 citations in OpenAlex.

  1. Study ofInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. NovelImmune network · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. STAT3 gain-of-function syndrome.Frontiers in pediatrics · 2022
    Review
  17. Article
  18. Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Lisa R ForbesaSection of Immunology, Department of Pediatrics, Allergy and Rheumatology, Baylor College of Medicine, Texas Children's Hospital Center for Human Immunobiology, Houston, Texas bNational Institutes of Health, Genetics and Pathogenesis of Allergy Section, Laboratory of Allergic Diseases, NIAID, Bethesda, Maryland, USA cDepartment of Pediatrics and Department of Microbiology, Immunology and Infectiology, University of Montreal, CHU Sainte-Justine Research Centre, Montreal, Quebec, Canada *Josh Milner and Elie Haddad share the senior authorship to the writing of this article.
Josh Milner
Elie Haddad
National Institutes of Health · USTexas Children's Hospital · USUniversité de Montréal · CA

Funding

Genetic and Pathophysiologic Study of Atopic DiseaseZIAAI001183 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MILNER, JOSHUA · 2013 to 2019
$8.7M
Pathogenesis and Treatment of Atopic DermatitisZIAAI001098 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MILNER, JOSHUA · 2009 to 2019
$6.5M
Intramural NIH HHS ZIA AI001098
6 · The paper itself

Abstract

purpose of reviewSignal transducer and activator of transcription 3 (STAT3) is an important transcription factor involved in a wide variety of cellular functions. Germline loss-of-function mutations are known to cause hyper-IgE immunodeficiency (autosomal dominant hyper IgE syndrome), whereas somatic gain-of-function mutations have been described in large granular cell leukemia, and polymorphisms in STAT3 have been associated with inflammatory bowel disease and other solid organ tumors. The review examines recent discoveries in our understanding of the nonmalignant disease processes affected by STAT3 mutations in human disease. RECENT

findingsGermline STAT3 gain-of-function mutations have recently been identified in patients with an early-onset autoimmunity/lymphoproliferative syndrome. STAT3 plays a previously unrecognized role in several facets of the pathogenesis of allergy. Loss-of-function STAT3 mutations revealed critical roles for STAT3 in the development and function of several lymphocyte populations and in their role in host defense. SUMMARY: The discovery of new gain-of-function mutations in STAT3, as well as new studies among patients with loss-of-function mutations, expand the understanding of the pathophysiology of STAT3 function and its importance in regulating the immune system. These findings contribute to elucidating STAT3 biology and clinical symptoms in patients with the different disease phenotypes.

Indexed as

Signal TransductionAnimalsAntibodiesAutoimmunityB-Lymphocyte SubsetsCytotoxicity, ImmunologicHumansHypersensitivityImmunologic MemoryInfectionsInterleukin-17Killer Cells, NaturalLymphoproliferative DisordersMutationSTAT3 Transcription FactorTh17 CellsAntibodiesInterleukin-17STAT3 Transcription Factor

Identifiers

PMID26574998
PMCPMC4790836
OpenAlexW2335963744

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.