Conditional neutrophil depletion challenges their contribution to mouse models of anaphylaxis.

Our data demonstrate that IgG-anaphylaxis can still occur in neutropenic mice and that neutrophil-targeting mAbs likely protect from anaphylaxis through their capacity to desensitize effector cells by engaging Fc Rs and inducing the release of PAF, rather than via neutrophil depletion I per se i . In humans, it is largely accepted that anaphylaxis relies predominately on IgE antibodies.[1] However, IgG might also contribute to anaphylaxis induced by infused drugs.[1] Several mouse models have been developed to identify key effector cells and mediators of anaphylaxis. [Extracted from the article]