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Related Concept Videos

Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by transmural...
Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy01:30

Inflammatory Bowel Disease III: Diagnostic Studies and Management I-Nutritional Therapy

Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
Diagnostic studies
A colonoscopy is the definitive screening test, distinguishing ulcerative colitis from other colon diseases with similar symptoms. During a colonoscopy test, inflamed mucosa with exudate ulcerations can be observed, and biopsies are taken to determine the histologic characteristics of the colonic...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

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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Related Experiment Video

Updated: Jul 27, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

The B-cell system in inflammatory bowel disease.

Per Brandtzaeg1, Hege S Carlsen, Trond S Halstensen

  • 1Laboratory for Immunohistochemistry and Immunopathology (LIIPAT), Institute of Pathology, University of Oslo, Norway.

Advances in Experimental Medicine and Biology
|April 20, 2006
PubMed
Summary

Secretory immunity, crucial for mucosal defense, is impaired in inflammatory bowel disease (IBD). Reduced immunoglobulin A (IgA) and altered IgA subclasses lead to compromised mucosal integrity and potential autoimmune responses in IBD.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Mucosal Immunity

Background:

  • Secretory immunity, a key component of the mucosal immune system, relies on the coordinated action of secretory epithelia and plasma cells.
  • Immunocytes produce polymeric immunoglobulin A (pIgA) and pentameric IgM, which bind to the epithelial secretory component (SC) via the polymeric immunoglobulin receptor (pIgR).
  • Secretory IgA (SIgA) and secretory IgM (SIgM) are essential for immune exclusion, preventing microbial colonization and antigen penetration at mucosal surfaces.

Purpose of the Study:

  • To investigate the alterations in secretory immunity, specifically immunoglobulin A (IgA) production and secretory component (SC) expression, in the context of inflammatory bowel disease (IBD).
  • To explore the implications of these changes on mucosal defense mechanisms and the potential role in autoimmune responses within IBD lesions.

Main Methods:

  • Analysis of J-chain expression in local plasma cells to assess pIgA production.
  • Evaluation of pIgR/SC expression in epithelial cells.
  • Assessment of IgA subclass distribution (IgA1 vs. IgA2) and IgG-producing cells.
  • Investigation of complement activation and its association with epithelium-bound IgG1 in ulcerative colitis.
  • Consideration of genetic factors and oral tolerance in the context of IBD pathogenesis.

Main Results:

  • A significant down-regulation of local pIgA production, evidenced by decreased J-chain expression, was observed in IBD.
  • Reduced pIgR/SC expression in regenerating and dysplastic epithelium indicates topical deficiency of the SIgA system.
  • A shift from IgA2 to the more proteolytically susceptible IgA1 subclass, increased IgG-producing cells, and macrophage activation suggest a 'frustrated' local immune response.
  • Complement activation, particularly involving epithelium-bound IgG1 in ulcerative colitis, points to autoimmune attack on the epithelial surface.
  • Evidence suggests a genetically determined skewed local IgG1 response in ulcerative colitis.
  • Massive microbial stimulation of the local B-cell system, potentially through abrogation of oral tolerance, is implicated in B-cell driven immunopathology.

Conclusions:

  • The secretory immune system is topically deficient in IBD, characterized by reduced IgA production and altered IgA subclasses.
  • The observed immune alterations contribute to compromised mucosal integrity and may involve autoimmune mechanisms, particularly in ulcerative colitis.
  • Microbial dysbiosis and a potential breakdown of oral tolerance likely play a significant role in initiating B-cell immunopathology in IBD.