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

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...

You might also read

Related Articles

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

Sort by
Same author

Precise Exchange of the Helper-Component Proteinase Cistron Between <i>Soybean mosaic virus</i> and <i>Clover yellow vein virus</i>: Impact on Virus Viability and Host Range Specificity.

Phytopathology·2019
Same author

No preventive or therapeutic efficacy of infliximab against macrophage activation syndrome due to systemic juvenile idiopathic arthritis.

Scandinavian journal of rheumatology·2018
Same author

Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice.

Science (New York, N.Y.)·2018
Same author

Genetic diversity does not explain variation in extra-pair paternity in multiple populations of a songbird.

Journal of evolutionary biology·2015
Same author

Do female parasitoid wasps recognize and adjust sex ratios to build cooperative relationships?

Journal of evolutionary biology·2012
Same author

The role of Staphylococcal enterotoxin in atopic keratoconjunctivitis and corneal ulceration.

Allergy·2012
Same journal

Corrigendum.

The Journal of allergy and clinical immunology·2026
Same journal

Comparative Efficacy of Biologic Agents for Severe Chronic Rhinosinusitis with Nasal Polyps: A Systematic Review and Network Meta-analysis.

The Journal of allergy and clinical immunology·2026
Same journal

Tamoxifen-driven neutrophil reprogramming protects from pulmonary Granulibacter bethesdensis infection in chronic granulomatous disease.

The Journal of allergy and clinical immunology·2026
Same journal

Clinical and transcriptomic characterization of mixed granulocytic COPD phenotype.

The Journal of allergy and clinical immunology·2026
Same journal

Dupilumab outcomes in pediatric asthma by early eosinophil status: post hoc analysis of VOYAGE/EXCURSION.

The Journal of allergy and clinical immunology·2026
Same journal

Maternal antibiotic exposure alters the newborn metabolomic profile and increases the risk of respiratory infections in offspring: a 13-year longitudinal birth cohort study.

The Journal of allergy and clinical immunology·2026
See all related articles

Related Experiment Video

Updated: Jun 22, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

Published on: April 9, 2018

Classical pathway complement activation in Kawasaki syndrome

T Kohsaka1, J Abe, T Asahina

  • 1National Childrens' Hospital, Childrens' Medical Research Center, Department of Immunology, Tokyo, Japan.

The Journal of Allergy and Clinical Immunology
|February 1, 1994
PubMed
Summary
This summary is machine-generated.

Complement activation via the classical pathway occurs in Kawasaki syndrome, indicated by breakdown products. Increased production of complement components compensates for activation, maintaining normal serum levels during inflammation.

More Related Videos

Application of Unsupervised Multi-Omic Factor Analysis to Uncover Patterns of Variation and Molecular Processes Linked to Cardiovascular Disease
08:51

Application of Unsupervised Multi-Omic Factor Analysis to Uncover Patterns of Variation and Molecular Processes Linked to Cardiovascular Disease

Published on: September 20, 2024

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Related Experiment Videos

Last Updated: Jun 22, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

Published on: April 9, 2018

Application of Unsupervised Multi-Omic Factor Analysis to Uncover Patterns of Variation and Molecular Processes Linked to Cardiovascular Disease
08:51

Application of Unsupervised Multi-Omic Factor Analysis to Uncover Patterns of Variation and Molecular Processes Linked to Cardiovascular Disease

Published on: September 20, 2024

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Area of Science:

  • Immunology
  • Pediatric Medicine
  • Complement System

Background:

  • Kawasaki syndrome is an acute febrile illness affecting young children.
  • The complement system plays a crucial role in innate and adaptive immunity.
  • Understanding complement activation in Kawasaki syndrome is vital for disease management.

Purpose of the Study:

  • To investigate complement activation pathways in patients with Kawasaki syndrome.
  • To examine the relationship between complement components and cytokine levels.
  • To determine if complement consumption occurs during the inflammatory process.

Main Methods:

  • Measurement of complement breakdown products (C3d, C4d, Bb, MAC) in patient plasma.
  • Assessment of hemolytic titers and intact complement protein concentrations (C3, C4, B).
  • Correlation analysis between serum cytokine levels (IL-6) and complement components.

Main Results:

  • Strong evidence of classical complement pathway activation was observed.
  • No significant decrease in hemolytic titer or intact complement proteins (C3, C4, B) was detected.
  • Elevated interleukin-6 levels correlated with C3 and B concentrations 5 days later.

Conclusions:

  • Complement activation via the classical pathway is implicated in Kawasaki syndrome.
  • Increased production of complement components accompanies the inflammatory response.
  • Activation products increase without a net decrease in serum complement levels due to compensatory production.