Expression of the high affinity IgE receptor by neutrophils of individuals with allergic asthma is both minimal and insensitive to regulation by serum IgE

被引:18
|
作者
Mora, Juanita [1 ]
Riggs, Emily K. [1 ]
Fu, Jun [1 ]
MacGlashan, Donald W., Jr. [2 ]
Fox, Susan A. [1 ]
Yu, Byung [1 ,3 ]
Tobin, Mary C. [1 ]
Thomas, Larry L. [1 ]
机构
[1] Rush Univ, Med Ctr, Dept Immunol Microbiol, Sect Allergy & Immunol, Chicago, IL 60612 USA
[2] Johns Hopkins Univ, Sch Med, Dept Med, Div Clin Immunol, Baltimore, MD 21205 USA
[3] John H Stroger Hosp Cook Cty, Chicago, IL USA
关键词
Allergic asthma; Neutrophils; Basophils; High affinity IgE receptor; IgE antibody; Fc receptors; FC-EPSILON-RI; HUMAN BASOPHILS; ANTIBODY; MODULATION; OMALIZUMAB; EXPOSURE; SURVIVAL; PROTEIN; ALPHA; CELLS;
D O I
10.1016/j.clim.2009.03.513
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We evaluated the hypothesis that serum IgE regulates neutrophil Fc epsilon RI expression in the same manner as described for other Fc epsilon RI+ cells. Fc epsilon RI expression by neutrophils of 40 asthma subjects and 20 control subjects did not correlate with serum IgE levels, whereas Fc epsilon RI expression by basophils of the same subjects showed a highly significant correlation. The level of Fc epsilon RI expression by neutrophils of both asthma and control subjects was approximately 1% of that for basophil Fc epsilon RI expression. IgE(+) neutrophils were minimally detectable, and Fc epsilon RI alpha-subunit was not detected in Western blots of neutrophil membranes and cytosol. The neutrophil Fc epsilon RI did not support anti-IgE stimulated superoxide release or IgE-induced increase in neutrophil survival. We conclude that Fc epsilon RI expression by neutrophils of both asthma patients and control individuals is minimal at best and that, if present, neutrophil Fc epsilon RI expression, unlike that of other human Fc epsilon RI+ cells, is not regulated by serum IgE. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:132 / 140
页数:9
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