ArticleProceedings of the National Academy of Sciences of the United States of America1998
T helper type 2 inflammatory disease in the absence of interleukin 4 and transcription factor STAT6.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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.
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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.
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Who cites it
46 citing papers in PubMed, 146 citations in OpenAlex.
- STAT Signature Dish: Serving Immunity with a Side of Dietary Control.Biomolecules · 2025Review
- Bcl6 and Blimp1 reciprocally regulate ST2The Journal of allergy and clinical immunology · 2020Article
- Blimp-1 is essential for allergen-induced asthma and Th2 cell development in the lung.The Journal of experimental medicine · 2020Article
- Dynamic repression by BCL6 controls the genome-wide liver response to fasting and steatosis.eLife · 2019Article
- Development of chronic allergic responses by dampening Bcl6-mediated suppressor activity in memory T helper 2 cells.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Follicular helper T cells mediate IgE antibody response to airborne allergens.The Journal of allergy and clinical immunology · 2017Article
- Review
- The transcriptional repressor Bcl6 controls the stability of regulatory T cells by intrinsic and extrinsic pathways.Immunology · 2015Article
- Deficiency of the transcriptional repressor B cell lymphoma 6 (Bcl6) is accompanied by dysregulated lipid metabolism.PloS one · 2014Article
- Insights into the role of Bcl6 in follicular Th cells using a new conditional mutant mouse model.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- STAT6 and lung inflammation.JAK-STAT · 2013Review
- The Bcl6 target gene microRNA-21 promotes Th2 differentiation by a T cell intrinsic pathway.Molecular immunology · 2013Article
- Lineage-specific functions of Bcl-6 in immunity and inflammation are mediated by distinct biochemical mechanisms.Nature immunology · 2013Article
- Bcl6 controls the Th2 inflammatory activity of regulatory T cells by repressing Gata3 function.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- The BTB-ZF transcription factors.Cell cycle (Georgetown, Tex.) · 2012Review
- Memory CD4+ T cells: fate determination, positive feedback and plasticity.Cellular and molecular life sciences : CMLS · 2012Review
- Identification of Bcl-6-dependent follicular helper NKT cells that provide cognate help for B cell responses.Nature immunology · 2011Article
- An alternate STAT6-independent pathway promotes eosinophil influx into blood during allergic airway inflammation.PloS one · 2011Article
- The infectious march: the complex interaction between microbes and the immune system in asthma.Immunology and allergy clinics of North America · 2010Review
- The Blimp1-Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis.The Journal of experimental medicine · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An important signaling pathway for the differentiation of T helper type 2 (TH2) cells from uncommitted CD4 T cell precursors is activation of the STAT6 transcription factor by interleukin 4 (IL-4). The protooncogene BCL-6 is also involved in TH2 differentiation, as BCL-6 -/- mice develop an inflammation of the heart and lungs associated with an overproduction of TH2 cells. Surprisingly, IL-4 -/- BCL-6 -/- and STAT6 -/- BCL-6 -/- double-mutant mice developed the same TH2-type inflammation of the heart and lungs as is characteristic of BCL-6 -/- mice. Furthermore, a TH2 cytokine response developed in STAT6 -/- BCL-6 -/- and IL-4 -/- BCL-6 -/- mice after immunization with a conventional antigen in adjuvant. In contrast to these in vivo findings, STAT6 was required for the in vitro differentiation of BCL-6 -/- T cells into TH2 cells. BCL-6, a transcriptional repressor that can bind to the same DNA binding motifs as STAT transcription factors, seems to regulate TH2 responses in vivo by a pathway independent of IL-4 and STAT6.
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Registered trials
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.