scholarly journals IgE-Mediated Systemic Anaphylaxis And Its Association With Gene Polymorphisms Of ACE, Angiotensinogen And Chymase

2019 ◽  
Vol Volume 12 ◽  
pp. 343-361 ◽  
Author(s):  
Veronica A Varney ◽  
Alex Nicholas ◽  
Amena Warner ◽  
Nazira Sumar
2011 ◽  
Vol 127 (3) ◽  
pp. 795-805.e6 ◽  
Author(s):  
Clinton B. Mathias ◽  
Suejy A. Hobson ◽  
Maria Garcia-Lloret ◽  
Greg Lawson ◽  
Dimitri Poddighe ◽  
...  

2018 ◽  
Vol 19 (5) ◽  
pp. 1279 ◽  
Author(s):  
Joseph Kulinski ◽  
Richard Proia ◽  
Elisabeth Larson ◽  
Dean Metcalfe ◽  
Ana Olivera

2018 ◽  
Vol 141 (2) ◽  
pp. AB192
Author(s):  
Andrew T. Dang ◽  
Yanfen Yang ◽  
Lisa Waggoner ◽  
Amnah Yamani ◽  
Taeko Noah ◽  
...  

2011 ◽  
Vol 127 (2) ◽  
pp. AB245-AB245
Author(s):  
C.B. Mathias ◽  
S.A. Hobson ◽  
M. Garcia-Lloret ◽  
G. Lawson ◽  
D. Poddighe ◽  
...  

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Hajime Karasuyama ◽  
Yusuke Tsujimura ◽  
Kazushige Obata ◽  
Kaori Mukai ◽  
Hideto Nishikado ◽  
...  

1999 ◽  
Vol 189 (10) ◽  
pp. 1573-1579 ◽  
Author(s):  
Azusa Ujike ◽  
Yoko Ishikawa ◽  
Masao Ono ◽  
Takae Yuasa ◽  
Tadashi Yoshino ◽  
...  

It is widely accepted that immunoglobulin (Ig)E triggers immediate hypersensitivity responses by activating a cognate high-affinity receptor, FcεRI, leading to mast cell degranulation with release of vasoactive and proinflammatory mediators. This apparent specificity, however, is complicated by the ability of IgE to bind with low affinity to Fc receptors for IgG, FcγRII and III. We have addressed the in vivo significance of this interaction by studying IgE-mediated passive systemic anaphylaxis in FcγR-deficient mice. Mice deficient in the inhibitory receptor for IgG, FcγRIIB, display enhanced IgE-mediated anaphylactic responses, whereas mice deficient in an IgG activation receptor, FcγRIII, display a corresponding attenuation of IgE-mediated responses. Thus, in addition to modulating IgG-triggered hypersensitivity responses, FcγRII and III on mast cells are potent regulators of IgE-mediated responses and reveal the existence of a regulatory pathway for IgE triggering of effector cells through IgG Fc receptors that could contribute to the etiology of the atopic response.


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