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Related Concept Videos

T Cell Types and Functions01:24

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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GPCRs Regulate Adenylyl Cylase Activity01:09

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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
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Related Experiment Video

Updated: Oct 19, 2025

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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GPR120 Inhibits Colitis Through Regulation of CD4+ T Cell Interleukin 10 Production.

Wenjing Yang1, Han Liu2, Leiqi Xu2

  • 1Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas.

Gastroenterology
|September 18, 2021
PubMed
Summary

G protein-coupled receptor 120 (GPR120) regulates T cells to produce interleukin 10, reducing intestinal inflammation. Targeting GPR120 offers a potential therapy for inflammatory bowel diseases.

Keywords:
Blimp1Effector CD4(+) T cellsGlycolysisInflammatory Bowel DiseasesIntestinal Homeostasis

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Investigating Target Gene Function in a CD40 Agonistic Antibody-induced Colitis Model using CRISPR/Cas9-based Technologies
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Area of Science:

  • Immunology
  • Gastroenterology
  • Metabolic Syndrome

Background:

  • G protein-coupled receptor (GPR) 120 is known for its anti-inflammatory effects in metabolic syndromes.
  • The specific role of GPR120 in intestinal inflammation, particularly its impact on T cells, remains largely unexplored.

Purpose of the Study:

  • To investigate the function of GPR120 in regulating CD4+ T cell activity.
  • To determine if GPR120 plays a role in the development and progression of colitis.
  • To explore the therapeutic potential of GPR120 agonists in treating intestinal inflammation.

Main Methods:

  • Utilized dextran sodium sulfate (DSS)-induced colitis, Citrobacter rodentium infection, and CD4+ T cell adoptive transfer mouse models.
  • Analyzed CD4+ T cell function using RNA sequencing, flow cytometry, and Seahorse metabolic assays.
  • Administered GPR120 agonist (CpdA) to assess its protective and therapeutic effects on colitis.

Main Results:

  • GPR120 deficiency in CD4+ T cells exacerbated colitis severity.
  • GPR120 agonists promoted IL-10 production in CD4+ T cells by upregulating Blimp1 and enhancing glycolysis via mTOR.
  • GPR120 agonist treatment protected mice from colitis and showed a positive correlation between GPR120 and IL-10 expression in human colonic mucosa.

Conclusions:

  • GPR120 plays a critical role in suppressing intestinal inflammation by enhancing IL-10 production in CD4+ T cells.
  • GPR120 represents a promising therapeutic target for inflammatory bowel diseases.