Related Experiment Video

Updated: Jun 20, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Complement cascade in systemic lupus erythematosus: analyses of the three activation pathways

Angela Ceribelli1, Laura Andreoli, Ilaria Cavazzana

  • 1Microbiology Institute, Ospedale San Carlo Borromeo, Milan, Italy. dott.ceribelli@libero.it

Annals of the New York Academy of Sciences
|September 18, 2009
PubMed

Insights

Complement (C") reduction correlates with disease activity in systemic lupus erythematosus (SLE). This study found a significant link between classical pathway (CP) activation and lupus activity, suggesting C

Area of Science:

  • Immunology
  • Rheumatology

Background:

  • The complement cascade is crucial for innate immunity, involving classical (CP), alternative (AP), and mannose-binding lectin (MP) pathways.
  • Complement reduction is a hallmark of systemic lupus erythematosus (SLE), contributing to pathogenesis and disease relapse.

Purpose of the Study:

  • To correlate complement (C') variations with SLE disease activity.
  • To investigate complement deficiencies in SLE patients.
  • To assess the utility of ELISA assays for SLE complement testing.

Main Methods:

  • Analysis of 52 serum samples from 20 SLE patients.
  • Testing of all three complement pathways (CP, AP, MP).
  • Correlation analysis using ECLAM score and anti-dsDNA antibodies.

Main Results:

  • A significant correlation was found between the ECLAM score and classical pathway (CP) activation (P = 0.001).
  • Correlation with anti-dsDNA antibodies did not reach statistical significance (P > 0.05).
  • A significant association between lupus activity phases and CP reduction was detected.

Conclusions:

  • The ELISA assay is suitable for testing complement levels in SLE samples.
  • Complement (C') reduction, particularly of the classical pathway (CP), is significantly linked to SLE disease activity.
  • Monitoring complement levels can aid in managing SLE flares.

More Related Videos

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice12:04

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Published on: November 1, 2015

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...
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...
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
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...