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The Role of Complement in Antibody Therapy for Infectious Diseases

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  • Authors: Peter P. Wibroe1, Shen Y. Helvig2, S. Moein Moghimi3
  • Editors: James E. Crowe Jr.4, Diana Boraschi5, Rino Rappuoli6
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Centre for Pharmaceutical Nanotechnology and Nanotoxicology, Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, DK-2100 Copenhagen Ø, Denmark; 2: Centre for Pharmaceutical Nanotechnology and Nanotoxicology, Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, DK-2100 Copenhagen Ø, Denmark; 3: Centre for Pharmaceutical Nanotechnology and Nanotoxicology, Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, DK-2100 Copenhagen Ø, Denmark; 4: Vanderbilt University School of Medicine, Nashville, TN; 5: National Research Council, Pisa, Italy; 6: Novartis Vaccines, Siena, Italy
  • Source: microbiolspec April 2014 vol. 2 no. 2 doi:10.1128/microbiolspec.AID-0015-2014
  • Received 19 February 2014 Accepted 27 February 2014 Published 11 April 2014
  • S. MoeinMoghimi, moien.moghimi@sund.ku.dk
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  • Abstract:

    The complement system is part of the innate immune system, eliciting central immunoregulatory functions. Detection of foreign surfaces is either achieved through complement-specific patternrecognition molecules or mediated by antigen recognition of antibodies. Immunoglobulin A (IgA), IgG, and IgM all have the potential to initiate a complement response, with the efficiency and response development closely related to the antibody isotype, multimeric state, and degree of glycosylation. A group of serum proteins constitutes the central effector functions of complement, thus allowing direct cell lysis, opsonization, and inflammation. These effector functions can be used in antibody therapies, especially against infectious diseases, as the target membranes lack complement regulatory proteins. The relative contribution of each function and the interplay with direct antibody-mediated clearance is not fully exploited, thus suggesting an option for further rational optimization of antibody therapies.

  • Citation: Wibroe P, Helvig S, Moein Moghimi S. 2014. The Role of Complement in Antibody Therapy for Infectious Diseases. Microbiol Spectrum 2(2):AID-0015-2014. doi:10.1128/microbiolspec.AID-0015-2014.

Key Concept Ranking

Complement System
0.6406026
Innate Immune System
0.5153678
Adaptive Immune System
0.5148315
Tumor Necrosis Factor alpha
0.5102202
0.6406026

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2014-04-11
2017-09-26

Abstract:

The complement system is part of the innate immune system, eliciting central immunoregulatory functions. Detection of foreign surfaces is either achieved through complement-specific patternrecognition molecules or mediated by antigen recognition of antibodies. Immunoglobulin A (IgA), IgG, and IgM all have the potential to initiate a complement response, with the efficiency and response development closely related to the antibody isotype, multimeric state, and degree of glycosylation. A group of serum proteins constitutes the central effector functions of complement, thus allowing direct cell lysis, opsonization, and inflammation. These effector functions can be used in antibody therapies, especially against infectious diseases, as the target membranes lack complement regulatory proteins. The relative contribution of each function and the interplay with direct antibody-mediated clearance is not fully exploited, thus suggesting an option for further rational optimization of antibody therapies.

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FIGURE 1

Schematic representation of complement activation by pathogens. The diagram shows the role of surface-bound antibodies and other complement-sensing molecules in complement triggering. Serum IgA is monomeric, but IgA in secretions is dimeric. IgM is pentameric. P, properdin; AP, alternative pathway. doi:10.1128/microbiolspec.AID-0015-2014.f1

Source: microbiolspec April 2014 vol. 2 no. 2 doi:10.1128/microbiolspec.AID-0015-2014
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FIGURE 2

Antibody-mediated pathogen attack and elimination mechanisms. doi:10.1128/microbiolspec.AID-0015-2014.f2

Source: microbiolspec April 2014 vol. 2 no. 2 doi:10.1128/microbiolspec.AID-0015-2014
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