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

Cellular Injury IlI: Cellular Death

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

Cytotoxic Edema: Pathophysiology

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

Regulation of Hematopoietic Stem Cells

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...

Cellular Injury IV: Necrosis

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

Overview of Cell Death

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...

You might also read

Related Articles

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

Sort by

Same author

Inflammatory conditions determine glucocorticoid effects on spontaneous or immunoglobulin-induced neutrophil death.

Pharmacology·2026

Same author

Glucagon-Like Peptide-1 Receptor Agonists as a Potential Mitochondrial Modulation Therapy for Hidradenitis Suppurativa.

Acta dermato-venereologica·2026

Same author

Molecular Characterization of Non-Specific Esophagitis Reveals a Distinct Non-Eosinophilic Phenotype With Fibrotic Traits.

Allergy·2026

Same author

An Immunologic Perspective on Adverse Reactions Observed Upon Systemic Therapies of Atopic Dermatitis: A Retrospective Study of 145 Cases.

Allergy·2026

Same author

Cytosolic proliferating cell nuclear antigen (PCNA) orchestrates neutrophil hyperactivation in COVID-19.

Proceedings of the National Academy of Sciences of the United States of America·2025

Same author

Blood group O expression in normal tissues and tumors.

The FEBS journal·2025

Search research articles

Related Experiment Video

Updated: Jun 13, 2026

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation

Published on: December 26, 2017

Cell death modulation by intravenous immunoglobulin.

Stephan von Gunten¹, Hans-Uwe Simon

¹Institute of Pharmacology, University of Bern, Friedbühlstrasse 49, Bern, Switzerland.

Journal of Clinical Immunology

|April 21, 2010

Summary

Intravenous immunoglobulin (IVIG) utilizes antibodies to induce immune cell death or protect tissue cells, impacting inflammatory disorders. This review explores IVIG

Area of Science:

Immunology
Pharmacology
Cell Biology

Background:

Naturally occurring antibodies in intravenous immunoglobulin (IVIG) can induce immune cell death or protect tissue cells.
These effects are mediated through interactions with death receptors, influencing inflammatory processes.
IVIG is recognized for its therapeutic benefits in inflammatory conditions like toxic epidermal necrolysis.

Purpose of the Study:

To review recent findings on the role of functional antibodies targeting Fas, Siglec-8, and Siglec-9 receptors in IVIG-mediated cellular effects.
To examine factors influencing IVIG's therapeutic efficacy in inflammatory diseases.

Main Methods:

Literature review focusing on antibodies against specific death receptors (Fas, Siglec-8, Siglec-9).
Analysis of cellular mechanisms (cell survival and death) influenced by IVIG.

More Related Videos

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy

Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy

Published on: August 2, 2024

Related Experiment Videos

Last Updated: Jun 13, 2026

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation

Published on: December 26, 2017

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy

Quantification of Cytokine-Induced Cell Death in Human Colonic Organoids Using Live Fluorescence Microscopy

Published on: August 2, 2024

Examination of modulating factors in inflammatory disease contexts.

Main Results:

Functional antibodies against Fas, Siglec-8, and Siglec-9 play a key role in IVIG's ability to induce immune cell death or promote cell survival.
The interplay between these antibodies and target cell status, cytokine environment, disease factors, genetics, and IVIG batch variations influences therapeutic outcomes.

Conclusions:

IVIG's anti-inflammatory mechanisms involve complex interactions with death receptors on immune and tissue cells.
Understanding these cellular events and influencing factors is crucial for optimizing IVIG therapy in various inflammatory disorders.