The role of the complement system in innate immunity

  title={The role of the complement system in innate immunity},
  author={Horea G Rus and Cornelia D Cudrici and Florin Niculescu},
  journal={Immunologic Research},
Complement is a major component of innate immune system involved in defending against all the foreign pathogens through complement fragments that participate in opsonization, chemotaxis, and activation of leukocytes and through cytolysis by C5b-9 membrane attack complex. Bacterias and viruses have adapted in various ways to escape the complement activation, and they take advantage of the complement system by using the host complement receptors to infect various cells. Complement activation also… 

Complement and autoimmunity

Data from preclinical studies and initial clinical trials suggest that the modulation of the complement system could constitute a viable strategy for the treatment of autoimmune conditions in the decades to come.

Complement and Adaptive Immunity: Roles for the Anaphylatoxins C3a and C5a in Regulating Tumor Immunity

In this review, the most recent evidence illustrating the role of the complement system in adaptive immunity and cancer will be discussed, and some questions will be raised as to whether some complement components can enhance the efficacy of cancer immunotherapy due to their influence on adaptive immunity.

Complement Deficiencies in Systemic Lupus Erythematosus

The goal of this review will be to discuss the associations between and the causal mechanisms of complement deficiencies and systemic lupus erythematosus.

Complement: an overview for the clinician.

On the Functional Overlap between Complement and Anti-Microbial Peptides

Because of the therapeutic implications, this review will consider closely studies dealing with complement activation and anti-microbial peptide activity in acute inflammation (e.g., dialysis-related peritonitis, appendicitis, and ischemia).

Targeting complement cascade: an alternative strategy for COVID-19

Pre-clinical and clinical studies evidence that the inhibition of complement components results in reduced complement deposits on target and non-target tissues, and aid in recovery from the pathological conditions of ARDS.

Targeted complement inhibition and microvasculature in transplants: a therapeutic perspective

The mechanism that complement contributes to angiogenic injury, and the development of future therapeutic targets by antagonizing activated complement mediators to preserve microvasculature in rejecting the transplanted organ are discussed.

Complement membrane attack complex is an immunometabolic regulator of NLRP3 activation and IL-18 secretion in human macrophages

Altered glycolytic flux and mitochondrial morphology and function mediate NLRP3 inflammasome activation, pro-inflammatory cytokine release and gasdermin D formation and elucidate a novel signalling cascade in MAC-stimulated human macrophages that drives an inflammatory consequence in an immunologically relevant cell type.

Formation and Maturation of the Phagosome: A Key Mechanism in Innate Immunity against Intracellular Bacterial Infection

The immune evasion strategies used by pathogens to regulate phagosome maturation during intracellular bacterial infection are discussed and it is indicated that these might be used for the development of potential therapeutic strategies for infectious diseases.

Complement, infection, and autoimmunity.

The relationship between the complement system and autoimmunity appears paradoxical as both the deficiency and the activation contribute to inducing autoimmune diseases.



The role of complement in B cell activation and tolerance.

Myeloid C3 Determines Induction of Humoral Responses to Peripheral Herpes Simplex Virus Infection 1

Insight is offered into the generation of the adaptive immune response in the periphery and a unique role is described for a nonhepatic complement source during the induction of humoral responses to peripheral HSV infection.

Impact of mannose-binding lectin on susceptibility to infectious diseases.

  • D. EisenR. Minchinton
  • Biology, Medicine
    Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • 2003
Clinical studies have shown that MBL insufficiency is associated with bacterial infection in patients with neutropenia and meningococcal sepsis, and low MBL levels appear to predispose persons to HIV infection.

Chemotaxis Inhibitory Protein of Staphylococcus aureus, a Bacterial Antiinflammatory Agent

A new protein secreted by Staphylococcus aureus is described that specifically impairs the response of neutrophils and monocytes to formylated peptides and C5a, suggesting a new immune escape mechanism of S. aUREus and putting forward CHIPS as a potential new antiinflammatory therapeutic compound.

Inhibition of C5a-induced inflammation with preserved C5b-9-mediated bactericidal activity in a human whole blood model of meningococcal sepsis.

The anti-C5a mAb 137-26 inhibits the potentially harmful effects of N meningitidis-induced C5a formation while preserving complement-mediated bacterial killing in a novel human whole blood model of meningococcal sepsis.

Complement-dependent Clearance of Apoptotic Cells by Human Macrophages

In the presence of serum, the macrophage receptors for C3bi, CR3 and CR4, were significantly more efficient in the uptake of apoptotic cells compared with previously described receptors implicated in clearance.

C1q Knock-Out Mice for the Study of Complement Deficiency in Autoimmune Disease

  • M. Botto
  • Biology, Medicine
    Experimental and Clinical Immunogenetics
  • 1998
Observations are compatible with the hypothesis that C1q deficiency causes autoimmunity by an impaired clearance of apoptotic cells.

A protective role for innate immunity in autoimmune disease.

  • M. Carroll
  • Biology, Medicine
    Clinical immunology
  • 2000
Systemic lupus erythematosus is an incurable autoimmune disease characterized by autoantibodies directed against highly conserved nuclear proteins and DNA. While the cause of lupus is not known,