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...
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...
Antibody Actions01:26

Antibody Actions

Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
Neutralization
Antibodies can bind to pathogens, preventing them from infecting host cells. This process...
Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
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,...
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...

You might also read

Related Articles

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

Sort by
Same author

Heparin-induced thrombocytopenia immune complexes activate the inflammasome pathway in a complement-dependent manner.

Journal of thrombosis and haemostasis : JTH·2026
Same author

Truncated complement factor H Y402 gene therapy rescues C3 glomerulonephritis.

Molecular therapy : the journal of the American Society of Gene Therapy·2025
Same author

Truncated Complement Factor H Y402 Gene Therapy Cures C3 Glomerulonephritis.

bioRxiv : the preprint server for biology·2024
Same author

Analysis of cold activation of the contact system in hereditary angioedema with normal C1 inhibitor.

Molecular immunology·2021
Same author

US HAEA Medical Advisory Board 2020 Guidelines for the Management of Hereditary Angioedema.

The journal of allergy and clinical immunology. In practice·2020
Same author

sgp120 and the contact system in hereditary angioedema: A diagnostic tool in HAE with normal C1 inhibitor.

Molecular immunology·2020
Same journal

Differential gene expression of retrotransposons (LTR and non-LTR) in peripheral blood leukocytes of people with gout.

Arthritis research & therapy·2026
Same journal

Alterations in systemic and skeletal muscle myostatin regulation are most prominent at disease onset and associate with muscle-related outcomes in idiopathic inflammatory myopathies.

Arthritis research & therapy·2026
Same journal

Plasma proteome differences between giant cell arteritis and polymyalgia rheumatica: a pilot study.

Arthritis research & therapy·2026
Same journal

Elucidating the mechanism of taurine in alleviating osteoarthritis progression based on bioinformatics, machine learning algorithm, and experimental validation.

Arthritis research & therapy·2026
Same journal

Discovery of biomarkers for primary Sj ögren's syndrome based on multi-omics data, construction of diagnostic models, and clinical correlation analysis.

Arthritis research & therapy·2026
Same journal

Identification of distinct subgroups in Chinese patients with Behçet's syndrome via cluster analysis of immune cells and clinical features.

Arthritis research & therapy·2026
See all related articles

Related Experiment Video

Updated: Jul 7, 2026

In Vivo Imaging Uncovers the Migratory Behavior of Leukocytes within the Joints
10:10

In Vivo Imaging Uncovers the Migratory Behavior of Leukocytes within the Joints

Published on: December 9, 2025

Complement and arthritis: another step in understanding.

Michael M Frank, C Garren Hester

    Arthritis Research & Therapy
    |February 29, 2008
    PubMed
    Summary
    This summary is machine-generated.

    Complement C4 binding protein deficiency does not impact autoimmune disease in MRL/lpr mice, suggesting the alternative pathway drives progression. However, classic pathway deficiency worsens renal pathology in milder lpr/lpr models.

    More Related Videos

    An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
    07:37

    An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

    Published on: June 6, 2025

    Related Experiment Videos

    Last Updated: Jul 7, 2026

    In Vivo Imaging Uncovers the Migratory Behavior of Leukocytes within the Joints
    10:10

    In Vivo Imaging Uncovers the Migratory Behavior of Leukocytes within the Joints

    Published on: December 9, 2025

    An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
    07:37

    An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

    Published on: June 6, 2025

    Area of Science:

    • Immunology
    • Autoimmune Diseases
    • Complement System

    Background:

    • The complement system, crucial for innate and adaptive immunity, comprises classic and alternative pathways.
    • The MRL/lpr mouse model exhibits systemic autoimmune disease, frequently used to study lupus.
    • C4 binding protein (C4BP) is a key regulator of the classic complement pathway.

    Discussion:

    • Wenderfer et al. investigated the role of C4BP in MRL/lpr mice, finding no effect on autoimmune disease development despite C4BP's role in down-regulating the classic pathway.
    • This aligns with prior research implicating the alternative complement pathway in driving MRL/lpr disease progression.
    • A discrepancy arises in the milder lpr/lpr mouse model, where classic pathway deficiency exacerbates renal pathology and disease severity.

    Key Insights:

    • C4BP deficiency does not influence autoimmune disease in the standard MRL/lpr mouse model.
    • Alternative complement pathway activation appears to be the primary driver of autoimmune disease in this model.
    • Classic pathway function is critical for mitigating renal pathology in milder MRL/lpr variants.

    Outlook:

    • Further research is needed to elucidate the specific factors contributing to the differing roles of the classic pathway in various MRL/lpr models.
    • Understanding these pathway-specific contributions could reveal novel therapeutic targets for autoimmune diseases.
    • Investigating the interplay between complement pathways and genetic background is essential for a comprehensive understanding of autoimmune pathogenesis.