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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >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.
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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.

机译：嵌合人猫Fcgamma-Fel d1融合蛋白抑制对主要猫过敏原Fel d1敏感的小鼠对气管内攻击的全身，肺和皮肤过敏反应。

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摘要

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.
机译：FcepsilonRI与FcgammaRIIb的共聚集可以通过将FcgammaRIIb与结合到FcepsilonRI的过敏原特异性IgE共交联来阻断FcepsilonRI介导的反应性和Fcγ：过敏原嵌合蛋白，从而可以阻断过敏原特异性反应性。我们评估了由与主要猫变应原（Fel d1）融合的部分人Ig G1 Fc组成的人猫嵌合融合蛋白（GFD）是否可作为变应原免疫疗法，而不会在对Fel d1致敏的小鼠中诱发急性过敏反应。在Fel d1攻击前6小时注射GFD会严重阻断Fel d1攻击的全身和皮肤反应，而在第37、38和39天接受GFD皮下免疫治疗的小鼠在2周内对Fel d1的全身，肺和皮肤反应均受到抑制后来。 GFD免疫疗法未引起全身反应。总体而言，Fcgamma-Fel d1嵌合融合蛋白阻断了Fel d1诱导的IgE介导的反应性，但自身并未诱导体内介质的释放。提示使用变应原与Fc gamma1结合以实现抑制信号转导的这种方法可能会提供增强形式的变应原免疫疗法。

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