ArticleThe Journal of experimental medicine1999
Alteration of interleukin 4 production results in the inhibition of T helper type 2 cell-dominated inflammatory bowel disease in T cell receptor alpha chain-deficient mice.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 88 citations in OpenAlex.
- Article
- Recent updates on the basic mechanisms and pathogenesis of inflammatory bowel diseases in experimental animal models.Intestinal research · 2020Review
- Genome-wide association studies of inflammatory bowel disease in German shepherd dogs.PloS one · 2018Article
- Contributions of the intestinal microbiome in lung immunity.European journal of immunology · 2018Review
- Cytokine Networks and T-Cell Subsets in Inflammatory Bowel Diseases.Inflammatory bowel diseases · 2016Review
- Galectin-3 suppresses mucosal inflammation and reduces disease severity in experimental colitis.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Endometrial regenerative cells as a novel cell therapy attenuate experimental colitis in mice.Journal of translational medicine · 2014Article
- Effects of interleukin-4 or interleukin-10 gene therapy on trinitrobenzenesulfonic acid-induced murine colitis.BMC gastroenterology · 2013Article
- NHE8 plays an important role in mucosal protection via its effect on bacterial adhesion.American journal of physiology. Cell physiology · 2013Article
- Animal models of ulcerative colitis and their application in drug research.Drug design, development and therapy · 2013Review
- Changes of the cytokine profile in inflammatory bowel diseases.World journal of gastroenterology · 2012Review
- Role of tumor necrosis factor-alpha (C-863A) polymorphism in pathogenesis of inflammatory bowel disease in Northern India.Journal of gastrointestinal cancer · 2012Article
- The membrane-bound mucin Muc1 regulates T helper 17-cell responses and colitis in mice.Gastroenterology · 2012Article
- Intestinal epithelial cells modulate CD4 T cell responses via the thymus leukemia antigen.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Loss of T cell and B cell quiescence precedes the onset of microbial flora-dependent wasting disease and intestinal inflammation in Gimap5-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Scorpion venom and the inflammatory response.Mediators of inflammation · 2010Review
- Gene expression patterns in experimental colitis in IL-10-deficient mice.Inflammatory bowel diseases · 2009Article
- Thymus leukemia antigen controls intraepithelial lymphocyte function and inflammatory bowel disease.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Role of cytokines in inflammatory bowel disease.World journal of gastroenterology · 2008Review
- Lymphocyte-dependent and Th2 cytokine-associated colitis in mice deficient in Wiskott-Aldrich syndrome protein.Gastroenterology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell receptor alpha chain-deficient (TCR-alpha(-/-)) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4(+)TCR-betabeta (CD4(+)betabeta) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4(+)betabeta T cells, we treated TCR-alpha(-/-) mice with anti-IL-4 monoclonal antibody (mAb). Approximately 60% of TCR-alpha(-/-) mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti-IL-4 mAb-treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab-treated mice. Although TCR-alpha(-/-) mice treated with either specific or mock Ab developed CD4(+)betabeta T cells, only those treated with anti-IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon gamma-specific expression. These findings suggest that IL-4-producing Th2-type CD4(+)betabeta T cells play a major immunopathological role in the induction of IBD in TCR-alpha(-/-) mice, a role that anti-IL-4 mAb inhibits by causing Th2-type CD4(+)betabeta T cells to shift to the Th1 type.
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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.