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

2.6K
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...
2.6K
T Cell Types and Functions01:24

T Cell Types and Functions

1.3K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.3K
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

1.5K
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...
1.5K
Antimicrobial Proteins01:23

Antimicrobial Proteins

3.7K
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...
3.7K
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

70.1K
Overview
70.1K
Inflammatory Response01:28

Inflammatory Response

5.4K
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,...
5.4K

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

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

Trained immunity in cardiovascular disease.

European heart journal·2025
Same author

Nitrate metabolism and periodontal health: The roles of nitric oxide in microbial killing and immunoregulation.

Periodontology 2000·2025
Same author

'Complement-ing' tissue inflammation via granzyme K?

Nature immunology·2025
Same journal

Crystal structure and immune single-cell atlas provide insights into the functional divergence of type I IFNs in fish.

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

Complement C3 deficiency increases the effector and cytotoxic functions of NK cells and suppresses tumor growth.

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

Increased Nur77 is disconnected from TCR affinity in insulin-specific Tregs.

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

FTR85 negatively regulates type I IFN antiviral signaling pathway by promoting K48-linked polyubiquitination of IRF3.

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

An MR1-specific nanobody capable of blocking MR1T cell activation.

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

TGF-β controls developmental fate and functional identity of thymic γδ T cells.

Journal of immunology (Baltimore, Md. : 1950)·2026
See all related articles

Related Experiment Video

Updated: Aug 30, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

11.6K

Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis.

Hui Wang1, Hidetaka Ideguchi1,2, Tetsuhiro Kajikawa1,3

  • 1Department of Basic and Translational Sciences, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA.

Journal of Immunology (Baltimore, Md. : 1950)
|August 26, 2022
PubMed
Summary
This summary is machine-generated.

Complement activation links oral microbiota to Th17 cells in periodontitis. This pathway drives inflammation and bone loss, highlighting a key mechanism in this inflammatory disease.

More Related Videos

Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
05:07

Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network

Published on: February 16, 2016

11.0K
Inducing Apical Periodontitis in Mice
10:26

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

12.3K

Related Experiment Videos

Last Updated: Aug 30, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

11.6K
Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
05:07

Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network

Published on: February 16, 2016

11.0K
Inducing Apical Periodontitis in Mice
10:26

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

12.3K

Area of Science:

  • Immunology
  • Oral Biology
  • Microbiology

Background:

  • Periodontitis is linked to complement and Th17 cells, involving systemic disorders.
  • Complement C3 inhibitor AMY-101 shows promise in resolving periodontal inflammation.

Purpose of the Study:

  • To dissect the cooperation between complement and Th17 cells in periodontitis development.
  • To understand how microbial dysbiosis triggers immune responses in the periodontium.

Main Methods:

  • Ligature-induced periodontitis (LIP) model in mice.
  • Analysis of complement activation, cytokine production (IL-6, IL-23), Th17 cell expansion, and IL-17 expression.
  • Investigation of IL-6 receptor signaling and C3a receptor expression in gingival epithelial cells.

Main Results:

  • Microbiota-induced complement activation in LIP mice generated IL-6 and IL-23, crucial for Th17 cell expansion.
  • C3-deficient mice showed suppressed Th17 cells, IL-17, and bone loss compared to wild-type.
  • IL-6 signaling was essential for LIP-induced IL-17 and bone loss.
  • Gingival epithelial cells produced IL-6 upon C3a stimulation, linking complement to Th17 induction.

Conclusions:

  • Complement activation bridges the periodontal microbiota challenge to Th17 cell accumulation.
  • This study integrates complement- and Th17-driven immunopathology in periodontitis.
  • Findings reveal a novel mechanism of immune crosstalk in inflammatory oral diseases.