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Human Fcγ-receptor IIb modulates pathogen-specific versus self-reactive antibody responses in lyme arthritis.
Journal article

Human Fcγ-receptor IIb modulates pathogen-specific versus self-reactive antibody responses in lyme arthritis.

  • Danzer H Institute of Genetics, Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.
  • Glaesner J Institute of Medical Microbiology and Hygiene, University Regensburg, Regensburg, Germany.
  • Baerenwaldt A Laboratory for Cancer Immunotherapy, University Hospital Basel, Basel, Switzerland.
  • Reitinger C Institute of Genetics, Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.
  • Lux A Institute of Genetics, Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.
  • Heger L Department of Dermatology, Laboratory of Dendritic Cell Biology, University Hospital Erlangen, Erlangen, Germany.
  • Dudziak D Department of Dermatology, Laboratory of Dendritic Cell Biology, University Hospital Erlangen, Erlangen, Germany.
  • Harrer T Medical Department 3, University Hospital Erlangen, Erlangen, Germany.
  • Gessner A Institute of Medical Microbiology and Hygiene, University Regensburg, Regensburg, Germany.
  • Nimmerjahn F Institute of Genetics, Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.
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  • 2020-07-03
Published in:
  • eLife. - 2020
Fc-receptor
arthritis
autoimmunity
borrelia burgdorferi
humanized mouse
immunology
inflammation
mouse
English Pathogen-specific antibody responses need to be tightly regulated to generate protective but limit self-reactive immune responses. While loss of humoral tolerance has been associated with microbial infections, the pathways involved in balancing protective versus autoreactive antibody responses in humans are incompletely understood. Studies in classical mouse model systems have provided evidence that balancing of immune responses through inhibitory receptors is an important quality control checkpoint. Genetic differences between inbred mouse models and the outbred human population and allelic receptor variants not present in mice; however, argue for caution when directly translating these findings to the human system. By studying Borrelia burgdorferi infection in humanized mice reconstituted with human hematopoietic stem cells from donors homozygous for a functional or a non-functional FcγRIIb allele, we show that the human inhibitory FcγRIIb is a critical checkpoint balancing protective and autoreactive immune responses, linking infection with induction of autoimmunity in the human immune system.
Language
  • English
Open access status
gold
Identifiers
Persistent URL
https://sonar.ch/global/documents/98727
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