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Updated: Aug 8, 2026

A Method to Assess Fc-mediated Effector Functions Induced by Influenza Hemagglutinin Specific Antibodies
04:47

A Method to Assess Fc-mediated Effector Functions Induced by Influenza Hemagglutinin Specific Antibodies

Published on: February 23, 2018

[Activation-dependent expression of Fc gamma-receptors on glomerular mesangial cells]

J E Gessner1, H H Radeke, P Uciechowski

  • 1Abteilungen Immunologie und Transfusionsmedizin, Medizinischen Hochschule Hannover.

Immunitat Und Infektion
|April 1, 1995
PubMed

Insights

Resting mesangial cells can express CD16TM receptors upon IFN gamma induction, leading to IL-6 secretion when immune complexes bind. This allows in vivo study of Fc receptors in chronic glomerular inflammation.

Area of Science:

  • Immunology
  • Nephrology
  • Cell Biology

Context:

  • Mesangial cells (MCs) play a key role in kidney function and disease.
  • Interferon gamma (IFN gamma) is a cytokine with immunomodulatory effects.
  • Fc receptors mediate immune complex recognition and cellular responses.

Purpose:

  • To investigate the functional role of Fc gamma-RIIIa and gamma chain-associated Fc receptors in mesangial cells.
  • To explore the induction of CD16TM receptor expression and subsequent IL-6 secretion in MCs.
  • To enable in vivo studies of chronic glomerular inflammation using Fc epsilon RI-gamma gene knockout models.

Summary:

  • IFN gamma induces resting mesangial cells to express Fc gamma-RIIIa and Fc epsilon RI-gamma subunits, forming the CD16TM receptor complex.
  • Binding of immune complexes to MCs expressing CD16TM triggers Interleukin-6 (IL-6) secretion.
  • The availability of Fc epsilon RI-gamma gene knockout models facilitates in vivo research on Fc receptor function in glomerular inflammation.

Impact:

  • Provides a novel in vitro system to study Fc receptor-mediated mesangial cell activation.
  • Enables detailed investigation into the role of Fc gamma-RIIIa in immune complex-induced kidney inflammation.
  • Facilitates the study of chronic glomerular inflammation within the intact immune system in vivo.

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