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Related Concept Videos

Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...

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Related Experiment Video

Updated: Jul 11, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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Inflammasomes and rheumatic diseases: evolving concepts.

P I Sidiropoulos1, G Goulielmos, G K Voloudakis

  • 1Department of Rheumatology, Clinical Immunology and Allergy, University Hospital, Medical School, University of Crete, Heraklion, Greece. sidiropp@med.uoc.gr

Annals of the Rheumatic Diseases
|October 9, 2007
PubMed
Summary
This summary is machine-generated.

Innate immunity, specifically nucleotide-binding and oligomerisation domain (NOD)-like receptors (NLRs) and inflammasomes, plays a key role in inflammatory rheumatic diseases. Targeting these pathways offers potential therapeutic strategies for conditions like rheumatoid arthritis and gout.

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Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • Inflammatory rheumatic diseases involve cytokine production triggered by endogenous signals.
  • Innate immunity mechanisms are increasingly recognized for their role in disease pathogenesis.
  • Nucleotide-binding and oligomerisation domain (NOD)-like receptors (NLRs) are key sensors in innate immunity.

Purpose of the Study:

  • To explore the role of NLRs and inflammasomes in the pathogenesis of inflammatory rheumatic diseases.
  • To understand how NLRs contribute to the initiation and progression of inflammation in rheumatic conditions.
  • To identify inflammasome pathways as potential therapeutic targets.

Main Methods:

  • Review of recent data on NLRs and inflammasome complexes.
  • Analysis of inflammasome components: NLR sensor, ASC adaptor, and caspase effector.
  • Investigation of inflammasome activation leading to pro-inflammatory cytokine release (IL-1β, IL-18).

Main Results:

  • NLRs are implicated in sensing cellular damage and endogenous metabolites.
  • Inflammasomes, comprising NLRs, ASC, and caspases, activate key inflammatory cytokines.
  • Evidence suggests inflammasome involvement in autoinflammatory and rheumatic diseases like rheumatoid arthritis and gout.

Conclusions:

  • The inflammasome pathway is a significant contributor to the pathogenesis of inflammatory rheumatic diseases.
  • Targeting NLRs and inflammasome signaling presents a promising therapeutic avenue.
  • Further research into these innate immunity pathways could lead to novel treatments for rheumatic conditions.