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Related Concept Videos

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

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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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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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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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Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids01:21

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Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
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Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

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Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
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Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy01:30

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Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
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In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction
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Immune cell therapy in IBD.

David Dunkin1, Saurabh Mehandru, Jean-Frédéric Colombel

  • 1Division of Gastroenterology and Institute of Immunology, Icahn School of Medicine at Mount Sinai, New York, N.Y., USA.

Digestive Diseases (Basel, Switzerland)
|December 23, 2014
PubMed
Summary
This summary is machine-generated.

Regulatory T cells (Tregs) offer a promising new therapy for inflammatory bowel disease (IBD). A recent clinical trial showed that Treg therapy was safe and effective for Crohn's disease patients refractory to other treatments.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cellular Therapy

Background:

  • Biologic therapies, particularly TNF inhibitors, have transformed IBD treatment but face challenges with non-response and secondary failure.
  • Advances in understanding regulatory T cells (Tregs) and their gut homing mechanisms enable novel cell-based therapies for IBD.
  • IBD can be viewed as an imbalance between pro-inflammatory Th17 cells and anti-inflammatory Tregs.

Purpose of the Study:

  • To explore ex vivo and in vivo strategies for enhancing Tregs in the gastrointestinal tract for IBD treatment.
  • To present findings from a phase 1/2a clinical trial investigating autologous ovalbumin-specific Tregs in Crohn's disease.

Main Methods:

  • A phase 1/2a clinical trial involving single escalating dose injections of autologous ovalbumin-specific Tregs in active Crohn's disease patients.
  • Investigation of intranasal and epicutaneous immunization methods to direct Tregs to the gastrointestinal tract.

Main Results:

  • The Treg therapy was well-tolerated in patients with active Crohn's disease.
  • The treatment demonstrated dose-related efficacy in patients refractory to conventional therapies.
  • Enhanced gut homing signatures of Tregs show potential for reducing gastrointestinal inflammation.

Conclusions:

  • Autologous ovalbumin-specific Treg therapy is a safe and potentially effective treatment for refractory Crohn's disease.
  • Strategies to enhance Treg gut homing offer a promising avenue for future IBD cell-based therapies.
  • Further research is needed to address the strengths and limitations of these novel therapeutic approaches in IBD.