Increased severity of local and systemic anaphylactic reactions in gp49B1-deficient mice.
Increased severity of local and systemic anaphylactic reactions in gp49B1-deficient mice.
复制标题
DOI：
10.1084/jem.194.2.227
复制
发表时间：
2001-07-16
期刊：
影响因子：
--
通讯作者：
Katz HR
中科院分区：
文献类型：
--
作者：
Daheshia M;Friend DS;Grusby MJ;Austen KF;Katz HR
gp49 B1是免疫球蛋白（IG）超家族成员，当两种受体与抗体在体外共连接时，其抑制Fcε RI诱导的肥大细胞活化。gp49B1的体内功能的关键问题现在在基因破坏的小鼠中得到解决。gp49B1缺陷小鼠表现出显着增加的IgE依赖性被动皮肤过敏反应的敏感性，更大的组织肿胀和肥大细胞脱粒原位评估。重要的是，根据相同的标准，gp49B1的缺乏也导致主动皮肤过敏反应中抗原激发的阈值较低，其中抗原特异性抗体水平在gp49B1缺陷和足够的小鼠中相当。此外，gp49B1的缺乏导致主动全身过敏反应的死亡率显著更高和更快。这些结果表明，gp49B1通过抑制肥大细胞活化在体内先天地抑制适应性速发型超敏反应。此外，本研究为过敏性疾病易感性和严重程度的调控提供了新的概念和靶点。
gp49B1 is an immunoglobulin (Ig) superfamily member that inhibits FcεRI-induced mast cell activation when the two receptors are coligated with antibodies in vitro. The critical question of in vivo function of gp49B1 is now addressed in gene-disrupted mice. gp49B1-deficient mice exhibited a significantly increased sensitivity to IgE-dependent passive cutaneous anaphylaxis as assessed by greater tissue swelling and mast cell degranulation in situ. Importantly, by the same criteria, the absence of gp49B1 also resulted in a lower threshold for antigen challenge in active cutaneous anaphylaxis, in which the antigen-specific antibody levels were comparable in gp49B1-deficient and sufficient mice. Moreover, the absence of gp49B1 resulted in a significantly greater and faster death rate in active systemic anaphylaxis. These results indicate that gp49B1 innately dampens adaptive immediate hypersensitivity responses by suppressing mast cell activation in vivo. In addition, this study provides a new concept and target for regulation of allergic disease susceptibility and severity.
登录
查看更多内容
影响因子：
15.9
作者：
MARTIN, TR;GALLI, SJ;DRAZEN, JM
通讯作者：
DRAZEN, JM
影响因子：
4.4
作者：
Matsumoto, Y;Wang, LL;Aso, T
通讯作者：
Aso, T
影响因子：
15.9
作者：
Miyajima, I;Dombrowicz, D;Galli, SJ
通讯作者：
Galli, SJ
影响因子：
3.2
作者：
McCormick, MJ;Castells, MC;Katz, HR
通讯作者：
Katz, HR
影响因子：
7.5
作者：
Habermann, Brunhilde Felding;Cheresh, David A.
通讯作者：
Cheresh, David A.