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一种人猫嵌合的Fcγ-Fel d1融合蛋白可抑制对主要猫过敏原Fel d1致敏的小鼠经气管内激发后的全身、肺部和皮肤过敏反应。

A chimeric human-cat Fcgamma-Fel d1 fusion protein inhibits systemic, pulmonary, and cutaneous allergic reactivity to intratracheal challenge in mice sensitized to Fel d1, the major cat allergen.

作者信息

Terada Tetsuya, Zhang Ke, Belperio John, Londhe Vedang, Saxon Andrew

机构信息

Department of Otorhinolaryngology, Osaka Medical College, Takatsuki, Osaka 569-8686, Japan.

出版信息

Clin Immunol. 2006 Jul;120(1):45-56. doi: 10.1016/j.clim.2005.12.010. Epub 2006 Feb 13.

Abstract

Co-aggregation of FcepsilonRI with FcgammaRIIb can block FcepsilonRI-mediated reactivity and Fc gamma:allergen chimeric proteins, by co-crosslinking FcgammaRIIb to allergen-specific IgE bound to the FcepsilonRI can block allergen-specific reactivity. We evaluated whether a human cat chimeric fusion protein (GFD) composed of part of the human Ig G1 Fc fused to the major cat allergen (Fel d1) would function as allergen immunotherapy while not inducing acute allergic reactivity in mice sensitized to Fel d1. Injection of GFD 6 h prior to Fel d1 challenge acutely blocked systemic and skin reactivity to Fel d1 challenge while mice given subcutaneous immunotherapy with GFD at days 37, 38, and 39 showed inhibition of systemic, lung, and cutaneous reactivity to Fel d1 2 weeks later. GFD immunotherapy did not induce systemic reactivity. Overall, the Fcgamma-Fel d1 chimeric fusion protein blocked Fel d1-induced IgE-mediated reactivity but did not induce in vivo mediator release on its own; suggesting that this approach using allergen combined with Fc gamma1 so as to achieve inhibitory signaling may provide an enhanced form of allergen immunotherapy.

摘要

FcεRI与FcγRIIb的共聚集可阻断FcεRI介导的反应性,并且通过将FcγRIIb与结合在FcεRI上的变应原特异性IgE共交联,Fcγ:变应原嵌合蛋白可阻断变应原特异性反应性。我们评估了一种由人Ig G1 Fc的一部分与主要猫变应原(Fel d1)融合而成的人-猫嵌合融合蛋白(GFD)是否能起到变应原免疫疗法的作用,同时又不会在对Fel d1致敏的小鼠中诱发急性过敏反应。在Fel d1激发前6小时注射GFD可急性阻断对Fel d1激发的全身和皮肤反应性,而在第37、38和39天接受GFD皮下免疫疗法的小鼠在2周后显示出对Fel d1的全身、肺部和皮肤反应性受到抑制。GFD免疫疗法未诱发全身反应性。总体而言,Fcγ-Fel d1嵌合融合蛋白阻断了Fel d1诱导的IgE介导的反应性,但自身并未在体内诱导介质释放;这表明这种将变应原与Fcγ1结合以实现抑制性信号传导的方法可能会提供一种增强型的变应原免疫疗法。

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