Abstract
We demonstrate that binding of different IgE molecules (IgEs) to their receptor, FcεRI, induces a spectrum of activation events in the absence of a specific antigen and provide evidence that such activation reflects aggregation of FcεRI. Highly cytokinergic IgEs can efficiently induce production of cytokines and render mast cells resistant to apoptosis in an autocrine fashion, whereas poorly cytokinergic IgEs induce these effects inefficiently. Highly cytokinergic IgEs seem to induce more extensive FcεRI aggregation than do poorly cytokinergic IgEs, which leads to stronger mast cell activation and survival effects. These effects of both types of IgEs require Syk tyrosine kinase and can be inhibited by FcεRI disaggregation with monovalent hapten. In hybridoma-transplanted mice, mucosal mast cell numbers correlate with serum IgE levels. Therefore, survival effects of IgE could contribute to the pathogenesis of allergic disease.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 12911-12916 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 100 |
| Issue number | 22 |
| DOIs | |
| State | Published - Oct 28 2003 |
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ASJC Scopus subject areas
- Genetics
- General
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Evidence that IgE molecules mediate a spectrum of effects on mast cell survival and activation via aggregation of the FcεRI. / Kitaura, Jiro; Song, Jinming; Tsai, Mindy; Asai, Koichi; Maeda-Yamamoto, Mari; Mocsai, Attila; Kawakami, Yuko; Liu, Fu-Tong; Lowell, Clifford A.; Barisas, B. George; Galli, Stephen J.; Kawakami, Toshiaki.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 100, No. 22, 28.10.2003, p. 12911-12916.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Evidence that IgE molecules mediate a spectrum of effects on mast cell survival and activation via aggregation of the FcεRI
AU - Kitaura, Jiro
AU - Song, Jinming
AU - Tsai, Mindy
AU - Asai, Koichi
AU - Maeda-Yamamoto, Mari
AU - Mocsai, Attila
AU - Kawakami, Yuko
AU - Liu, Fu-Tong
AU - Lowell, Clifford A.
AU - Barisas, B. George
AU - Galli, Stephen J.
AU - Kawakami, Toshiaki
PY - 2003/10/28
Y1 - 2003/10/28
N2 - We demonstrate that binding of different IgE molecules (IgEs) to their receptor, FcεRI, induces a spectrum of activation events in the absence of a specific antigen and provide evidence that such activation reflects aggregation of FcεRI. Highly cytokinergic IgEs can efficiently induce production of cytokines and render mast cells resistant to apoptosis in an autocrine fashion, whereas poorly cytokinergic IgEs induce these effects inefficiently. Highly cytokinergic IgEs seem to induce more extensive FcεRI aggregation than do poorly cytokinergic IgEs, which leads to stronger mast cell activation and survival effects. These effects of both types of IgEs require Syk tyrosine kinase and can be inhibited by FcεRI disaggregation with monovalent hapten. In hybridoma-transplanted mice, mucosal mast cell numbers correlate with serum IgE levels. Therefore, survival effects of IgE could contribute to the pathogenesis of allergic disease.
AB - We demonstrate that binding of different IgE molecules (IgEs) to their receptor, FcεRI, induces a spectrum of activation events in the absence of a specific antigen and provide evidence that such activation reflects aggregation of FcεRI. Highly cytokinergic IgEs can efficiently induce production of cytokines and render mast cells resistant to apoptosis in an autocrine fashion, whereas poorly cytokinergic IgEs induce these effects inefficiently. Highly cytokinergic IgEs seem to induce more extensive FcεRI aggregation than do poorly cytokinergic IgEs, which leads to stronger mast cell activation and survival effects. These effects of both types of IgEs require Syk tyrosine kinase and can be inhibited by FcεRI disaggregation with monovalent hapten. In hybridoma-transplanted mice, mucosal mast cell numbers correlate with serum IgE levels. Therefore, survival effects of IgE could contribute to the pathogenesis of allergic disease.
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UR - http://www.scopus.com/inward/citedby.url?scp=0242331616&partnerID=8YFLogxK
U2 - 10.1073/pnas.1735525100
DO - 10.1073/pnas.1735525100
M3 - Article
C2 - 14569021
AN - SCOPUS:0242331616
VL - 100
SP - 12911
EP - 12916
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 22
ER -