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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...
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...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
T Cell Types and Functions01:24

T Cell Types and Functions

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...
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...

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Related Experiment Video

Updated: May 18, 2026

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
12:04

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

Published on: November 1, 2015

Complement, interferon and lupus.

Keith B Elkon1, Deanna M Santer

  • 1Division of Rheumatology and Department of Immunology, University of Washington, Seattle, WA 98195, USA. elkon@u.washington.edu

Current Opinion in Immunology
|September 25, 2012
PubMed
Summary
This summary is machine-generated.

Complement deficiencies linked to lupus may stem from impaired clearance of immune complexes and apoptotic cells. This leads to increased interferon-alpha production, a key factor in lupus pathogenesis.

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Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α
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Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α

Published on: June 14, 2018

Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • The complement pathway is crucial in the immune system's response to pathogens and cellular debris.
  • Deficiencies in early complement components (C1q, C2, C4) are paradoxically linked to an increased risk of developing systemic lupus erythematosus (SLE).

Purpose of the Study:

  • To elucidate the mechanisms by which complement components, particularly C1q, influence the pathogenesis of lupus.
  • To explore the interplay between the complement system and type I interferon production in SLE.

Main Methods:

  • The study discusses findings related to immune complex (IC) and apoptotic cell clearance.
  • It examines the role of C1q in modulating the interaction between these entities and immune cells like plasmacytoid dendritic cells (pDCs) and monocytes.
  • The research also considers the impact of C1q on neutrophil extracellular traps (NETs).

Main Results:

  • Absence of C1q leads to preferential binding of immune complexes to pDCs, promoting interferon-alpha (IFN-α) production.
  • C1q-opsonized apoptotic cells normally exert immunosuppressive effects, which are lost in C1q deficiency.
  • C1q impedes the degradation of NETs, which are implicated in type I IFN production in SLE.

Conclusions:

  • Impaired clearance of immune complexes and apoptotic cells due to complement deficiencies, especially C1q, contributes to lupus pathogenesis.
  • These deficiencies promote type I IFN production through mechanisms involving pDCs and NETs.
  • The findings highlight a direct and indirect link between complement dysregulation and type I IFN signaling in SLE.