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Related Concept Videos

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...
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...
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

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 (Humira),...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

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 Disease...
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...
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Inflammatory Bowel Disease IV: Pharmacological Management

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: Jun 13, 2026

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

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Published on: April 21, 2015

Autoantibodies Drive Fcγ Receptor-Dependent Colon Inflammation During Immune Checkpoint Blockade.

Iryna Voloshyna1, Yury Patskovsky1, Sabina Sandigursky1

  • 1Laura and Isaac Perlmutter Cancer Center, New York University Grossman School of Medicine, New York, NY 10016, USA.

Biorxiv : the Preprint Server for Biology
|June 12, 2026
PubMed
Summary
This summary is machine-generated.

Endogenous autoantibodies (AAbs) promote immune checkpoint inhibitor (ICI)-associated colitis via Fc gamma receptor (FcγR) pathways. Humanized FcγR mice receiving patient IgG developed colon inflammation, revealing a targetable IgG-regulated inflammatory network.

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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

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Last Updated: Jun 13, 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

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
07:34

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Area of Science:

  • Immunology
  • Gastroenterology
  • Oncology

Background:

  • Immune checkpoint inhibitor (ICI) therapy is limited by immune-related adverse events (irAEs), especially colitis.
  • The precise mechanisms underlying ICI-associated colitis remain poorly understood.

Purpose of the Study:

  • To investigate the role of endogenous autoantibodies (AAbs) in promoting ICI-associated colitis.
  • To elucidate the Fc gamma receptor (FcγR)-dependent pathways involved in colitis development.

Main Methods:

  • Transfer of IgG from melanoma patients undergoing ICI therapy into wild-type and humanized FcγR (hFcγR) mice.
  • Administration of ICI therapy to recipient mice.
  • Analysis of colon inflammation, immune cell infiltration, cytokine profiles, and gene expression via single-cell RNA sequencing.
  • Autoantibody profiling of patient serum.

Main Results:

  • hFcγR mice receiving patient IgG developed significant colon inflammation, including lymphocyte infiltration and goblet cell loss.
  • ICI therapy combined with patient IgG induced circulating cytokines (IL-1β, IL-17a, IL-22) and an IgG-regulated inflammatory network.
  • This network involved specific immune cells like ILC1, Th1, cytotoxic T cells, M1 macrophages, B cells, and ILC3-LTi cells.
  • CCR5 and CXCR4 receptors were identified as potential targets associated with colitis susceptibility.

Conclusions:

  • Endogenous AAbs can drive ICI-associated colitis through FcγR-dependent mechanisms.
  • Targeting the identified IgG-regulated inflammatory network and receptors like CCR5/CXCR4 may offer therapeutic strategies for managing irAEs.