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Updated: Feb 14, 2026
04:47
A Method to Assess Fc-mediated Effector Functions Induced by Influenza Hemagglutinin Specific Antibodies
Published on: February 23, 2018
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Functional Fc gamma receptor gene polymorphisms and donor-specific antibody-triggered microcirculation inflammation
M L Arnold1, A Kainz2, L G Hidalgo3
1Department of Internal Medicine 3, Institute for Clinical Immunology, Friedrich-Alexander University, Erlangen-Nuremberg, Germany.
Summary
High-affinity Fc gamma receptor IIIA (FcγRIIIA) variants may increase inflammation in kidney transplant recipients with donor-specific antibodies (DSAs). This FcγRIIIA polymorphism is linked to microcirculation inflammation but not long-term kidney function.
Area of Science:
- Transplantation immunology
- Immunogenetics
Background:
- Fc-dependent effector mechanisms are implicated in antibody-mediated rejection (ABMR).
- Fc gamma receptor (FcγR) gene polymorphisms may influence donor-specific antibody (DSA)-triggered inflammation.
Purpose of the Study:
- To investigate the association between functional FcγR variants and late antibody-mediated rejection (ABMR) in kidney transplant recipients.
Main Methods:
- Genotyping of FcγRIIA, FcγRIIIA, and FcγRIIIB polymorphisms in 85 DSA-positive kidney allograft recipients.
- Analysis of peritubular capillaritis (ptc) in protocol biopsies.
- Assessment of kidney function over 24 months.
- In vitro functional assays using NK92 cells.
Main Results:
- High-affinity FCGR3A-V158 alleles (V/V158 or V/F158) were associated with a higher rate and extent of ptc (P=.018).
- These associations were independent of C1q-binding to DSA or capillary C4d.
- No significant differences in kidney function were observed over 24 months.
- NK92 cells expressing FCGR3A-V158 produced more interferon gamma when incubated with antibody-coated cells.
Conclusions:
- High-affinity FcγRIIIA variants may promote DSA-triggered microcirculation inflammation in kidney allografts.
- FcγRIIA and FcγRIIIB polymorphisms were not linked to allograft morphology.
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