Systemic anaphylaxis in the mouse can be mediated largely through IgG, and Fc gamma RIII - Assessment of the cardiopulmonary changes, mast cell degranulation, and death associated with active or IgE- or IgG(1)-dependent passive anaphylaxis
Systemic anaphylaxis in the mouse can be mediated largely through IgG, and Fc gamma RIII - Assessment of the cardiopulmonary changes, mast cell degranulation, and death associated with active or IgE- or IgG(1)-dependent passive anaphylaxis
复制标题
DOI：
10.1172/jci119255
复制
发表时间：
1997-03-01
影响因子：
15.9
通讯作者：
Galli, SJ
中科院分区：
文献类型：
--
作者：
Miyajima, I;Dombrowicz, D;Galli, SJ
我们尝试在缺乏 Fc(ε)RI α 链或 Fc(ε)RI 和 Fc γ RI/III 共有的 FcR γ 链的小鼠或缺乏肥大细胞的小鼠中引发对卵清蛋白的主动过敏反应，或被动 IgE 或 IgG(1) 依赖性过敏反应 （Kit(W)/Kit(W-v) 小鼠），并将反应与相应野生型小鼠的反应进行比较。我们发现 FcR γ 链是死亡以及大多数与主动过敏反应或 IgE 或 IgG(1) 依赖性被动过敏反应相关的病理生理变化所必需的。此外，Fc(ε)RI α链-/-小鼠中与主动或IgG(1)依赖性被动过敏反应相关的一些生理变化明显大于相应的正常小鼠。最后，虽然Kit(W)/Kit(W-v)和同类+/+小鼠均表现出致命的主动过敏反应，但肥大细胞缺陷小鼠在主动和IgG(1)依赖性被动全身过敏反应中均表现出比相应野生型小鼠更弱的生理反应。我们的研究结果强烈表明，虽然 IgE 抗体和 Fc(ε)RI 可能会影响与小鼠活动性过敏反应相关的一些病理生理变化的强度和/或动力学，但与这种反应相关的死亡率主要是由 IgG(1) 抗体和 Fc gamma-RIII 介导的。
We attempted to elicit active anaphylaxis to ovalbumin, or passive IgE- or IgG(1)-dependent anaphylaxis, in mice lacking either the Fc(epsilon)RI alpha chain or the FcR gamma chain common to Fc(epsilon)RI and Fc gamma RI/III, or in mice lacking mast cells (Kit(W)/Kit(W-v) mice), and compared the responses to those in the corresponding wild-type mice. We found that the FcR gamma chain is required for the death, as well as for most of the pathophysiological changes, associated with active anaphylaxis or IgE- or IgG(1)-dependent passive anaphylaxis. Moreover, some of the physiological changes associated with either active, or IgG(1)-dependent passive, anaphylactic responses were significantly greater in Fc(epsilon)RI alpha chain -/- mice than in the corresponding normal mice. Finally, while both Kit(W)/Kit(W-v) and congenic +/+ mice exhibited fatal active anaphylaxis, mast cell-deficient mice exhibited weaker physiological responses than the corresponding wild-type mice in both active and IgG(1)-dependent passive systemic anaphylaxis. Our findings strongly suggest that while IgE antibodies and Fc(epsilon)RI may influence the intensity and/or kinetics of some of the pathophysiological changes associated with active anaphylaxis in the mouse, the mortality associated with this response can be mediated largely by IgG(1) antibodies and Fc gamma-RIII.