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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...
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...
Protein Complex Assembly02:41

Protein Complex Assembly

Proteins can form homomeric complexes with another unit of the same protein or heteromeric complexes with different types.  Most protein complexes self-assemble spontaneously via ordered pathways, while some proteins need assembly factors that guide their proper assembly. Despite the crowded intracellular environment, proteins usually interact with their correct partners and form functional complexes.
Many viruses self-assemble into a fully functional unit using the infected host cell to...
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...
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...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...

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Related Experiment Video

Updated: Jun 15, 2026

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion
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Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

Interaction of pneumococcal histidine triad proteins with human complement.

Merit Melin1, Emmanuel Di Paolo, Leena Tikkanen

  • 1National Institute for Health and Welfare, Department of Vaccination and Immune Protection, Mannerheimintie 166, 00300 Helsinki, Finland. merit.melin@thl.fi

Infection and Immunity
|March 3, 2010
PubMed
Summary

Pneumococcal histidine triad (Pht) proteins may aid immune evasion, but their role in complement inhibition via Factor H binding is unlikely. Their function varies by genetic background and other pneumococcal proteins.

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Assays for Studying the Role of Vitronectin in Bacterial Adhesion and Serum Resistance

Published on: October 16, 2018

Area of Science:

  • Microbiology
  • Immunology
  • Vaccine Development

Background:

  • Pneumococcal histidine triad (Pht) proteins (PhtA, PhtB, PhtD, PhtE) are surface proteins of Streptococcus pneumoniae.
  • These proteins are targets for antibodies and potential vaccine candidates, showing promise in preclinical studies.
  • Their precise function in pneumococcal pathogenesis, particularly in evading the host immune system, remains unclear, with a potential role in complement inhibition suggested.

Purpose of the Study:

  • To investigate the role of Pht proteins in the inhibition of the host complement system.
  • To determine if Pht proteins mediate immune evasion through Factor H binding.
  • To assess the impact of Pht proteins on complement deposition across different Streptococcus pneumoniae strains and genetic backgrounds.

Main Methods:

  • Comparative analysis of complement C3 deposition on wild-type and Pht-deficient Streptococcus pneumoniae strains (serotypes 2, 3, 4, 19F, and R36A).
  • Measurement of Factor H binding to bacterial cells, lysates, and purified Pht antigens using flow cytometry and other assays.
  • Comparison of Pht mutants with single and double mutants of other surface proteins like PspA and PspC.

Main Results:

  • Deletion of all four Pht proteins (Pht(-)) led to increased C3 deposition specifically on the serotype 4 strain, but not on other tested strains.
  • Pht antigens did not directly bind Factor H, and their absence did not significantly alter Factor H binding to bacterial lysates.
  • The Pht(-) mutant serotype 4 strain exhibited slightly reduced Factor H binding compared to the wild-type strain.

Conclusions:

  • Pht proteins may contribute to immune evasion in Streptococcus pneumoniae, but not through direct Factor H binding.
  • The influence of Pht proteins on complement inhibition is strain-specific and likely modulated by other pneumococcal surface proteins and the bacterial genetic background.
  • Further research is needed to elucidate the exact mechanisms of Pht-mediated immune evasion.