Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Intracellular Signaling Affects Focal Adhesions

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...

Clot Retraction and Fibrinolysis

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

Inflammatory Response

Inflammatory Response

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,...

Formation of the Platelet Plug

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

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

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),...

You might also read

Related Articles

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

Sort by

Same author

Measuring performance trajectories in lung cancer surgery: a longitudinal study using the French national hospital database from 2020 to 2024.

BMJ health & care informatics·2026

Same author

Reducing Bias in the Evaluation of Robotic Surgery for Lung Cancer Through Machine Learning.

Cancers·2025

Same author

Monitoring anti-Rituximab antibodies in myasthenia gravis affects the time to event during Rituximab treatment.

Journal of neurology·2025

Same author

Immunosenescence markers in T- and NK-cells according to the CD4/CD8 ratio in successfully treated people living with HIV.

Frontiers in medicine·2025

Same author

DNA damage response regulator ATR licenses PINK1-mediated mitophagy.

Nucleic acids research·2025

Same author

Tumor-intrinsic and immune-related features associated with treatment failure in human papillomavirus-related oropharyngeal cancer.

Journal of the National Cancer Institute·2025

Search research articles

Related Experiment Video

Updated: Jul 15, 2026

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization

Published on: December 3, 2020

Interactions between CD47 and thrombospondin reduce inflammation.

Laurence Lamy¹, Arnaud Foussat, Eric J Brown

¹INSERM Unit 576, Hospitalier de l'Université de Nice, University of Nice-Sophia Antipolis, Hôpital de l'Archet I, 151 rue Saint Antoine de Ginestière, Nice, France.

Journal of Immunology (Baltimore, Md. : 1950)

|April 20, 2007

Summary

CD47 and thrombospondin (TSP) regulate T cell apoptosis to limit inflammation. Deficiencies in CD47 or TSP prolong inflammation by reducing T cell death, highlighting a new pathway for controlling immune responses.

More Related Videos

The Use of the Ex Vivo Chandler Loop Apparatus to Assess the Biocompatibility of Modified Polymeric Blood Conduits

The Use of the Ex Vivo Chandler Loop Apparatus to Assess the Biocompatibility of Modified Polymeric Blood Conduits

Published on: August 20, 2014

Related Experiment Videos

Last Updated: Jul 15, 2026

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization

Published on: December 3, 2020

The Use of the Ex Vivo Chandler Loop Apparatus to Assess the Biocompatibility of Modified Polymeric Blood Conduits

The Use of the Ex Vivo Chandler Loop Apparatus to Assess the Biocompatibility of Modified Polymeric Blood Conduits

Published on: August 20, 2014

Area of Science:

Immunology
Cell Biology

Background:

CD47 on T cells can induce activation or apoptosis, depending on thrombospondin (TSP) levels.
T cell apoptosis is crucial for resolving inflammation.

Purpose of the Study:

To investigate the in vivo role of the CD47/thrombospondin pathway in regulating T cell apoptosis and inflammation.
To elucidate the mechanism by which CD47 influences T cell apoptosis.

Main Methods:

Utilized CD47-deficient, TSP-1-deficient, and TSP-2-deficient mouse models.
Induced oxazolone inflammation to assess inflammatory responses and T cell apoptosis.
Examined the expression of BNIP3 (Bcl-2/adenovirus E1B 19-kDa interacting protein) in activated T cells.

Main Results:

CD47-, TSP-1-, or TSP-2-deficient mice exhibited prolonged oxazolone-induced inflammation (>4 days) compared to wild-type mice (<48 h).
Prolonged inflammation in deficient mice was associated with reduced local T cell apoptosis.
Activated T cells upregulate BNIP3 and undergo CD47-mediated apoptosis, with BNIP3 degradation inhibited by CD47.

Conclusions:

The CD47/BNIP3 pathway is critical in vivo for limiting inflammation by controlling activated T cell numbers.
This pathway promotes T cell apoptosis, thereby resolving inflammatory responses.
Findings reveal a novel mechanism for immune regulation involving CD47 and BNIP3.