Abstract
Mast cells play critical roles in hypersensitivity and in defense against certain parasites. We provide evidence that mouse mast cell survival and growth are promoted by monomeric IgE binding to its high-affinity receptor, FcεRI. Monomeric IgE does not promote DNA synthesis but suppresses the apoptosis induced by growth factor deprivation. This antiapoptotic effect occurs in parallel with IgE-induced increases in FcεRI surface expression but requires the continuous presence of IgE. This process does not involve the FasL/Fas death pathway or several Bcl-2 family proteins and induces a distinctly different signal than FcεRI cross-linking. The ability of IgE to enhance mast cell survival and FcεRI expression may contribute to amplified allergic reactions.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 791-800 |
| Number of pages | 10 |
| Journal | Immunity |
| Volume | 14 |
| Issue number | 6 |
| DOIs | |
| State | Published - 2001 |
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ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases
- Immunology
Cite this
Regulation of mast cell survival by IgE. / Asai, Koichi; Kitaura, Jiro; Kawakami, Yuko; Yamagata, Noboru; Tsai, Mindy; Carbone, David P.; Liu, Fu-Tong; Galli, Stephen J.; Kawakami, Toshiaki.
In: Immunity, Vol. 14, No. 6, 2001, p. 791-800.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Regulation of mast cell survival by IgE
AU - Asai, Koichi
AU - Kitaura, Jiro
AU - Kawakami, Yuko
AU - Yamagata, Noboru
AU - Tsai, Mindy
AU - Carbone, David P.
AU - Liu, Fu-Tong
AU - Galli, Stephen J.
AU - Kawakami, Toshiaki
PY - 2001
Y1 - 2001
N2 - Mast cells play critical roles in hypersensitivity and in defense against certain parasites. We provide evidence that mouse mast cell survival and growth are promoted by monomeric IgE binding to its high-affinity receptor, FcεRI. Monomeric IgE does not promote DNA synthesis but suppresses the apoptosis induced by growth factor deprivation. This antiapoptotic effect occurs in parallel with IgE-induced increases in FcεRI surface expression but requires the continuous presence of IgE. This process does not involve the FasL/Fas death pathway or several Bcl-2 family proteins and induces a distinctly different signal than FcεRI cross-linking. The ability of IgE to enhance mast cell survival and FcεRI expression may contribute to amplified allergic reactions.
AB - Mast cells play critical roles in hypersensitivity and in defense against certain parasites. We provide evidence that mouse mast cell survival and growth are promoted by monomeric IgE binding to its high-affinity receptor, FcεRI. Monomeric IgE does not promote DNA synthesis but suppresses the apoptosis induced by growth factor deprivation. This antiapoptotic effect occurs in parallel with IgE-induced increases in FcεRI surface expression but requires the continuous presence of IgE. This process does not involve the FasL/Fas death pathway or several Bcl-2 family proteins and induces a distinctly different signal than FcεRI cross-linking. The ability of IgE to enhance mast cell survival and FcεRI expression may contribute to amplified allergic reactions.
UR - http://www.scopus.com/inward/record.url?scp=0034948713&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034948713&partnerID=8YFLogxK
U2 - 10.1016/S1074-7613(01)00157-1
DO - 10.1016/S1074-7613(01)00157-1
M3 - Article
C2 - 11420048
AN - SCOPUS:0034948713
VL - 14
SP - 791
EP - 800
JO - Immunity
JF - Immunity
SN - 1074-7613
IS - 6
ER -