IgE Effector Mechanisms, in Concert with Mast Cells, Contribute to Acquired Host Defense against Staphylococcusaureus

IgE效应机制与肥大细胞协同作用,促进宿主获得性防御金黄色葡萄球菌感染。

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作者:Philipp Starkl ,Martin L Watzenboeck ,Lauren M Popov ,Sophie Zahalka ,Anastasiya Hladik ,Karin Lakovits ,Mariem Radhouani ,Arvand Haschemi ,Thomas Marichal ,Laurent L Reber ,Nicolas Gaudenzio ,Riccardo Sibilano ,Lukas Stulik ,Frédéric Fontaine ,André C Mueller ,Manuel R Amieva ,Stephen J Galli ,Sylvia Knapp

Abstract

Allergies are considered to represent mal-directed type 2 immune responses against mostly innocuous exogenous compounds. Immunoglobulin E (IgE) antibodies are a characteristic feature of allergies and mediate hypersensitivity against allergens through activation of effector cells, particularly mast cells (MCs). Although the physiological functions of this dangerous branch of immunity have remained enigmatic, recent evidence shows that allergic immune reactions can help to protect against the toxicity of venoms. Because bacteria are a potent alternative source of toxins, we assessed the possible role of allergy-like type 2 immunity in antibacterial host defense. We discovered that the adaptive immune response against Staphylococcus aureus (SA) skin infection substantially improved systemic host defense against secondary SA infections in mice. Moreover, this acquired protection depended on IgE effector mechanisms and MCs. Importantly, our results reveal a previously unknown physiological function of allergic immune responses, IgE antibodies, and MCs in host defense against a pathogenic bacterium.

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