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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...
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Related Experiment Video

Updated: Jan 10, 2026

Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1
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C1q and mannose-binding lectin binding and complement activation across genetically diverse Mycobacterium

Mario Alejandro Duque-Villegas1,2,3, Maximilian Peter Götz3, Emilie Rousseau2

  • 1Infection Immunology, Research Center Borstel, Borstel, Germany.

Journal of Immunology (Baltimore, Md. : 1950)
|November 20, 2025
PubMed
Summary

Complement system proteins C1q and mannose-binding lectin (MBL) recognize diverse Mycobacterium tuberculosis strains, activating complement. However, this activation doesn't kill the bacteria, revealing complex host-pathogen interactions.

Keywords:
Mycobacterium tuberculosis complexC1qMACMBLcomplement activation

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Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Tuberculosis (TB), caused by Mycobacterium tuberculosis complex (MTBC), is a major global health threat.
  • Genetic diversity within MTBC influences disease progression and host immune response.
  • The complement system, a key innate immunity component, has incompletely understood interactions with MTBC.

Purpose of the Study:

  • To investigate the roles of C1q and mannose-binding lectin (MBL) in complement activation against diverse MTBC strains.
  • To elucidate the contribution of these pattern recognition molecules (PRMs) in early host-pathogen dynamics during TB infection.

Main Methods:

  • Direct binding assays of C1q and MBL to clinical MTBC strains.
  • Assessment of complement cascade activation, including C4b/C3b deposition and membrane attack complex (MAC) formation.
  • Inhibition experiments using nonimmune serum to determine the primary drivers of complement activation.

Main Results:

  • Both C1q and MBL directly bind to MTBC strains in a strain-dependent manner.
  • C1q and MBL facilitate complement activation, leading to C4b/C3b deposition and MAC formation.
  • C1q is the primary activator in nonimmune serum, with MBL playing a supportive role; MAC formation does not significantly affect MTBC viability.

Conclusions:

  • The study reveals a complex interplay between complement system components (C1q, MBL) and MTBC genetic diversity.
  • Complement activation, while robust, does not confer direct bacterial killing, highlighting immune evasion mechanisms.
  • Understanding MTBC lineage diversity is crucial for comprehending immune responses and developing effective TB therapies.