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

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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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...
Antimicrobial Proteins01:23

Antimicrobial Proteins

Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
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...

You might also read

Related Articles

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

Sort by
Same author

Periodontal Medicine Rewired: Mechanisms Linking Periodontitis to Systemic Diseases.

Journal of periodontal research·2026
Same author

Bone marrow rewired: Trained immunity and clonal hematopoiesis in metabolic disease.

Metabolism: clinical and experimental·2026
Same author

DEL-1 is an Endogenous Senolytic Protein that Inhibits Senescence-Associated Bone Loss.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026
Same author

Inflammageing and clonal haematopoiesis interplay and their impact on human disease.

Nature reviews. Molecular cell biology·2026
Same author

Epigenetic inflammatory memory and periodontal disease: Mechanisms and clinical significance for comorbidities.

Journal of periodontology·2025
Same author

Trained immunity in cardiovascular disease.

European heart journal·2025

Related Experiment Video

Updated: Jun 16, 2026

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
09:51

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

Published on: July 26, 2017

Crosstalk pathways between Toll-like receptors and the complement system.

George Hajishengallis1, John D Lambris

  • 1University of Louisville School of Dentistry, Division of Oral Health and Systemic Disease, Louisville, KY, USA. g0haji01@louisville.edu

Trends in Immunology
|February 16, 2010
PubMed
Summary
This summary is machine-generated.

Toll-like receptors (TLRs) and complement are vital innate immunity components. Their crosstalk can enhance immune responses or control inflammation, but pathogens may exploit this interaction for survival.

More Related Videos

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

Related Experiment Videos

Last Updated: Jun 16, 2026

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling
09:51

Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

Published on: July 26, 2017

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment
07:26

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

Published on: July 18, 2017

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

Area of Science:

  • Immunology
  • Infectious Disease
  • Molecular Biology

Background:

  • Toll-like receptors (TLRs) and the complement system are crucial innate immune mechanisms.
  • These systems are typically studied independently, but recent findings reveal significant crosstalk between them.

Purpose of the Study:

  • To explore the intricate interplay between complement and TLR signaling pathways.
  • To understand how this crosstalk influences innate immunity and inflammation during infection.

Main Methods:

  • Review and analysis of existing scientific literature on complement and TLR signaling.
  • Examination of studies investigating the synergistic and antagonistic interactions between these pathways.

Main Results:

  • Evidence suggests complement-TLR interactions can either boost innate immunity or dampen excessive inflammation.
  • Pathogens can manipulate this crosstalk to promote their own persistence within the host.

Conclusions:

  • The interplay between complement and TLRs is complex, with dual roles in host defense and pathogen evasion.
  • Further research into these regulatory links is critical for understanding their roles in health and disease.