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Related Concept Videos

Antibody Structure01:10

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Overview
Antibodies, also known as immunoglobulins (Ig), are essential players of the adaptive immune system. These antigen-binding proteins are produced by B cells and make up 20 percent of the total blood plasma by weight. In mammals, antibodies fall into five different classes, which each elicits a different biological response upon antigen binding.
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Groups of proteins may form a complex where each protein in this complex has a different role in the overall execution of the complex’s function. Often some of the proteins in the complex can be replaced by a closely related variant to give a complex that contains many of the same components yet is functionally distinct.
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Related Experiment Video

Updated: Jan 16, 2026

A Method to Assess Fc-mediated Effector Functions Induced by Influenza Hemagglutinin Specific Antibodies
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Understanding mechanistic relationships between IgG titers and Fc effector functions: a computational framework to

Suzanne K Shoffner-Beck1, Robert M Theisen1, Kade E Wong1

  • 1Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, United States.

Frontiers in Immunology
|October 2, 2025
PubMed
Summary

Higher IgG titers may decrease antibody-dependent cellular functions (ADCC/ADCP). A computational model revealed complex interactions influencing immune responses, guiding future vaccine design.

Keywords:
antibody-dependent cellular cytotoxicity (ADCC)antibody-mediated effector functionshuman immunodeficiency virus (HIV)mechanistic modelordinary differential equation model

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Area of Science:

  • Immunology
  • Computational Biology
  • Vaccinology

Background:

  • Antibody-dependent cellular functions like ADCC and ADCP are crucial for vaccine and infectious disease immunity.
  • These functions involve complex interactions between IgG antibodies, Fc gamma receptors (FcγRs), and antigens, making experimental deconvolution challenging.

Purpose of the Study:

  • To develop a computational model predicting FcγRIIIa (ADCC) and FcγRIIa (ADCP) immune complexes.
  • To dissect mechanisms of immune complex formation and Fc effector function activation.

Main Methods:

  • Created an ordinary differential equation model to predict FcγRIIIa and FcγRIIa immune complexes.
  • Simulated vaccine boosts (IgG1, IgG3) in HIV vaccine trial participants using the model.

Main Results:

  • Model predicted maximum immune complex formation not at highest IgG titers; higher titers can decrease FcγRIIIa/FcγRIIa complexes due to competition.
  • Simulated IgG1 and IgG3 combination boosts showed no significant change in ADCC/ADCP complexes.
  • Simulated IgG3 boost alone significantly decreased ADCP (p<0.00001) but increased ADCC.

Conclusions:

  • A computational framework provides quantitative insights into Fc effector function activation.
  • This approach can guide the rational design of therapeutic and prophylactic interventions.