Impaired IgG-Dependent Anaphylaxis and Arthus Reaction in FcγRIII (CD16) Deficient Mice

@article{Hazenbos1996ImpairedIA,
  title={Impaired IgG-Dependent Anaphylaxis and Arthus Reaction in Fc$\gamma$RIII (CD16) Deficient Mice},
  author={Wouter L. W. Hazenbos and Johannes Engelbert Gessner and Frans M. A. Hofhuis and Henri Kuipers and D. Meyer and Ingmar A.F.M. Heijnen and Reinhold Ernst Schmidt and M{\'a}ty{\'a}s S{\'a}ndor and Peter J. A. Capel and Marc Da{\"e}ron and Jan G. J. Winkel and J. Sjef Verbeek},
  journal={Immunity},
  year={1996},
  volume={5},
  pages={181-188}
}
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TLDR
IgG‐mediated anaphylaxis is directly demonstrated and the blocking of FcγR would provide one of the therapeutic targets for the control of IgG‐ mediated hypersensitivity diseases.
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In insight into distinct signaling mechanisms in mast cells underlying the development of diverse pathologies as well as a therapeutic potential for selective treatment of allergic disorders, Lyn is not involved in the onset of the IgG-mediated, FcγRIII-dependent late phase responses of mast cells.
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TLDR
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Impact of CD40 Ligand, B Cells, and Mast Cells in Peanut-Induced Anaphylactic Responses1
TLDR
The data demonstrate that the presence of peanut-specific Abs along with functional MCs comprise a necessary and sufficient condition for the elicitation ofanut-induced anaphylaxis, and suggests that strategies to impair MC degranulation may be necessary to improve the efficacy of anti-IgE therapy.
C5a anaphylatoxin is a major regulator of activating versus inhibitory FcgammaRs in immune complex-induced lung disease.
TLDR
C5a, which is a potent chemoattractant, has a broader critical function in regulating the inhibitory/activating FcGammaRII/III receptor pair to connect complement and FcgammaR effector pathways in immune inflammation.
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It is reported that despite the IgE deficiency, sensitized mutant mice become anaphylactic on antigen challenge and display tachycardia and pulmonary function changes similar to those seen in wild-type animals, demonstrating that non-IgE pathways for hypersensi-tivity reactions exist in mice.
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