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Related Concept Videos

Inflammatory Response01:28

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,...
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Inflammation

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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...
Inflammation: Introduction01:28

Inflammation: Introduction

Inflammation is a fundamental, protective biological response of vascularized tissues to cellular injury, infection, or harmful stimuli. Its primary function is to eliminate the initial cause of injury, clear necrotic cells and damaged tissue, and initiate the necessary repair processes.Cardinal SignsAcute inflammation presents with classic signs. Redness results from vasodilation and increased blood flow. Heat is due to increased metabolism and circulation. Swelling results from the...
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...

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Updated: May 17, 2026

Stimulation of Cytoplasmic DNA Sensing Pathways In Vitro and In Vivo
11:44

Stimulation of Cytoplasmic DNA Sensing Pathways In Vitro and In Vivo

Published on: September 18, 2014

STING manifests self DNA-dependent inflammatory disease.

Jeonghyun Ahn1, Delia Gutman, Shinobu Saijo

  • 1Department of Cell Biology and Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, FL 33136, USA.

Proceedings of the National Academy of Sciences of the United States of America
|November 8, 2012
PubMed
Summary

Mice lacking DNase II experienced embryonic death due to undigested DNA activating inflammatory pathways. Blocking STING (Stimulator of Interferon Genes) prevented this, revealing STING

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Autoimmune diseases like SLE involve chronic cytokine overproduction, potentially triggered by self nucleic acids.
  • Mice lacking DNase II exhibit embryonic lethality due to impaired DNA digestion and activation of innate immune sensors.
  • The specific cellular pathways mediating DNA-induced inflammation in autoimmune conditions are not fully understood.

Purpose of the Study:

  • To identify the cellular sensor pathway responsible for DNA-mediated inflammation and embryonic lethality in DNase II-deficient mice.
  • To investigate the role of Stimulator of Interferon Genes (STING) in these inflammatory processes.

Main Methods:

  • Utilizing DNase II-deficient mouse models.
  • Employing genetic knockout strategies to assess the function of STING.
  • Analyzing cytokine production and inflammatory responses in vivo.

Main Results:

  • Stimulator of Interferon Genes (STING) was identified as the key mediator of inflammation-related embryonic death in DNase II-defective mice.
  • Loss of STING function rescued DNase II-dependent embryonic lethality.
  • STING deficiency completely prevented polyarthritis by inhibiting robust cytokine production triggered by cytosolic DNA.

Conclusions:

  • STING is a critical component of the cellular pathway linking self DNA to inflammatory autoimmune disease.
  • Targeting STING signaling offers a potential therapeutic strategy for preventing DNA-mediated inflammatory disorders.