Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

35
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...
35
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

1.8K
Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
1.8K
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

34
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...
34
Inflammatory Response01:28

Inflammatory Response

12.5K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
12.5K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

1.8K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
1.8K
T Cell Types and Functions01:24

T Cell Types and Functions

3.2K
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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

CEACAM5 as a biomarker of semi-solid, lepidic lung adenocarcinoma.

Translational lung cancer research·2026
Same author

Autophagy Inhibition Reprograms the Tumor Microenvironment of Pancreatic Cancer to Promote Macrophage Phagocytosis of Tumor Cells.

Cancer research·2026
Same author

TIGIT agonism as a therapeutic strategy to suppress inflammation in hidradenitis suppurativa.

Frontiers in immunology·2026
Same author

Early posttransplant rituximab use in kidney transplant recipients with preexisting donor-specific antibodies.

Renal failure·2026
Same author

B7-H3 as a Universal Target for Solid Tumor Therapy: Clinical Promise and Biological Complexity.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology·2025
Same author

A Framework for Assessing the Opportunity for Advanced Research, Development, and Regulatory Approval of Medical Countermeasures: A Component of BARDA's Emerging Infectious Diseases Strategy.

The Journal of infectious diseases·2025

Related Experiment Video

Updated: May 3, 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

16.5K

Tissue-expressed B7-H1 critically controls intestinal inflammation.

Lisa Scandiuzzi1, Kaya Ghosh1, Kimberly A Hofmeyer1

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Cell Reports
|February 18, 2014
PubMed
Summary

B7-H1, also known as PD-L1, expressed in the gut tissue, is crucial for preventing intestinal inflammation. Its absence in mice leads to severe gut injury and high mortality.

More Related Videos

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

2.5K
Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
09:25

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine

Published on: May 21, 2012

39.0K

Related Experiment Videos

Last Updated: May 3, 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

16.5K
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

2.5K
Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
09:25

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine

Published on: May 21, 2012

39.0K

Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • B7-H1 (PD-L1) on immune cells inhibits T-cell responses via PD-1.
  • The role of B7-H1 in the intestinal epithelium during inflammation was previously unclear.

Purpose of the Study:

  • To investigate the function of intestinal epithelial B7-H1 in regulating gut inflammation.
  • To determine the cellular source and mechanism of B7-H1's anti-inflammatory action in the gut.

Main Methods:

  • Utilized B7-H1-deficient mice in dextran sodium sulfate (DSS) and trinitrobenzenesulfonic acid (TNBS) induced colitis models.
  • Employed bone marrow chimeric and knockout mouse studies.
  • Analyzed cytokine production (TNF-α, IL-22) and bacterial overgrowth.

Main Results:

  • B7-H1-deficient mice exhibited severe susceptibility to DSS/TNBS-induced gut injury, with high mortality.
  • B7-H1 expression on intestinal parenchyma, not hematopoietic cells, controlled inflammation independently of adaptive immunity.
  • B7-H1 inhibited TNF-α and promoted IL-22 secretion from lamina propria cells.

Conclusions:

  • Intestinal epithelial B7-H1 is essential for preventing gut inflammation.
  • B7-H1 acts as a critical ligand for innate immune cells in the lamina propria.
  • This pathway involves regulating TNF-α and IL-22 to maintain intestinal homeostasis.