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

The Extrinsic Apoptotic Pathway01:17

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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Inflammation01:38

Inflammation

Overview
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...

You might also read

Related Articles

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

Sort by
Same author

TRIM21 facilitates inflammasome assembly and contributes to autoinflammatory disease.

Nature communications·2026
Same author

An overview of human inflammasomes: Activation and regulation.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

IL-17RC signaling connects intestinal microbiota and neuroimmune interactions in atherosclerosis.

bioRxiv : the preprint server for biology·2026
Same author

cGAS-STING dependent type I IFN reduces Leptospira interrogans renal colonization in mice.

PLoS pathogens·2026
Same author

The Nrf2 Activator CDDO-Imidazole Suppresses Inflammation-Induced Red Blood Cell Alloimmunization.

Antioxidants (Basel, Switzerland)·2025
Same author

Loss of Tripartite Motif-Containing Protein 21 and UVB-Induced Systemic Inflammation by Regulating DNA-Sensing Pathways.

Arthritis & rheumatology (Hoboken, N.J.)·2025

Related Experiment Video

Updated: Jun 6, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Inflammasomes and their activation.

Sonal Khare1, Nancy Luc, Andrea Dorfleutner

  • 1Division of Rheumatology, Department of Medicine and Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Critical Reviews in Immunology
|November 19, 2010
PubMed
Summary

The innate immune system uses pattern recognition receptors to detect pathogens and activate immune responses. This review focuses on Nod-like receptors and AIM2, crucial for inflammasome activation and controlling immunity and disease.

More Related Videos

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
09:04

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
08:41

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

Published on: April 6, 2022

Related Experiment Videos

Last Updated: Jun 6, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
09:04

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
08:41

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

Published on: April 6, 2022

Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • The innate immune system is the first line of defense against pathogens.
  • Pattern recognition receptors (PRRs) identify conserved molecular patterns on microbes.
  • Nod (nucleotide-binding oligimerization domain)-like receptors (NLRs) and AIM2 (absent in melanoma 2) are key PRRs involved in inflammasome activation.

Purpose of the Study:

  • To summarize recent advancements in understanding the function of Nod-like receptors in immunity.
  • To highlight the role of NLRs and AIM2 in inflammasome activation and its consequences.
  • To discuss the implications of NLR function in various diseases.

Main Methods:

  • Review of recent scientific literature on NLRs, AIM2, inflammasomes, and pyroptosis.
  • Analysis of studies investigating the molecular mechanisms of inflammasome activation.
  • Synthesis of data linking NLR function to immune responses and disease pathogenesis.

Main Results:

  • NLRs and AIM2 function as critical PRRs that assemble inflammasomes in macrophages.
  • Inflammasomes are essential for activating inflammatory caspases, leading to cytokine maturation and pyroptosis.
  • Dysregulation of NLR-mediated inflammasome activation is implicated in numerous inflammatory diseases.

Conclusions:

  • Nod-like receptors play a pivotal role in innate immunity by sensing danger signals and orchestrating inflammatory responses.
  • Targeting inflammasome pathways involving NLRs and AIM2 presents potential therapeutic strategies for inflammatory diseases.
  • Continued research into NLR function is vital for advancing our understanding of immune defense and disease mechanisms.