Abstract
Studies performed using cultured cells indicate that IgE functions not only to trigger degranulation of mast cells following allergen exposure, but also to enhance their survival. Such an influence of IgE on mast cell homeostasis during allergic responses in vivo has not been established. In this study, we show that inhalation of Aspergillus fumigatus extract in mice induced a dramatic rise in IgE accompanied by an increase in airway mast cells. These had an activated phenotype with high levels of FcεRI. Plasma mast cell protease-1 was also increased, indicating an elevated systemic mast cell load. In addition, enhanced levels of IL-5 and eosinophils were observed in the airway. Both mast cell expansion and activation were markedly attenuated in IgE-/- animals that are incapable of producing IgE in response to A. fumigatus. The recruitment of eosinophils to the airways was also reduced in IgE-/- mice. Analyses of potential cellular targets of IgE revealed that IgE Abs are not required for the induction of mast cell progenitors in response to allergen, but rather act by sustaining the survival of mature mast cells. Our results identify an important role for IgE Abs in promoting mast cell expansion during allergic responses in vivo.
| Original language | English |
|---|---|
| Pages (from-to) | 2416-2424 |
| Number of pages | 9 |
| Journal | Journal of Immunology |
| Volume | 182 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Feb 15 2009 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology
Cite this
IgE influences the number and function of mature mast cells, but not progenitor recruitment in allergic pulmonary inflammation. / Mathias, Clinton B.; Freyschmidt, Eva Jasmin; Caplan, Benjamin; Jones, Tatiana; Poddighe, Dimitri; Xing, Wei; Harrison, Krista L.; Gurish, Michael F.; Oettgen, Hans C.
In: Journal of Immunology, Vol. 182, No. 4, 15.02.2009, p. 2416-2424.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - IgE influences the number and function of mature mast cells, but not progenitor recruitment in allergic pulmonary inflammation
AU - Mathias, Clinton B.
AU - Freyschmidt, Eva Jasmin
AU - Caplan, Benjamin
AU - Jones, Tatiana
AU - Poddighe, Dimitri
AU - Xing, Wei
AU - Harrison, Krista L.
AU - Gurish, Michael F.
AU - Oettgen, Hans C.
PY - 2009/2/15
Y1 - 2009/2/15
N2 - Studies performed using cultured cells indicate that IgE functions not only to trigger degranulation of mast cells following allergen exposure, but also to enhance their survival. Such an influence of IgE on mast cell homeostasis during allergic responses in vivo has not been established. In this study, we show that inhalation of Aspergillus fumigatus extract in mice induced a dramatic rise in IgE accompanied by an increase in airway mast cells. These had an activated phenotype with high levels of FcεRI. Plasma mast cell protease-1 was also increased, indicating an elevated systemic mast cell load. In addition, enhanced levels of IL-5 and eosinophils were observed in the airway. Both mast cell expansion and activation were markedly attenuated in IgE-/- animals that are incapable of producing IgE in response to A. fumigatus. The recruitment of eosinophils to the airways was also reduced in IgE-/- mice. Analyses of potential cellular targets of IgE revealed that IgE Abs are not required for the induction of mast cell progenitors in response to allergen, but rather act by sustaining the survival of mature mast cells. Our results identify an important role for IgE Abs in promoting mast cell expansion during allergic responses in vivo.
AB - Studies performed using cultured cells indicate that IgE functions not only to trigger degranulation of mast cells following allergen exposure, but also to enhance their survival. Such an influence of IgE on mast cell homeostasis during allergic responses in vivo has not been established. In this study, we show that inhalation of Aspergillus fumigatus extract in mice induced a dramatic rise in IgE accompanied by an increase in airway mast cells. These had an activated phenotype with high levels of FcεRI. Plasma mast cell protease-1 was also increased, indicating an elevated systemic mast cell load. In addition, enhanced levels of IL-5 and eosinophils were observed in the airway. Both mast cell expansion and activation were markedly attenuated in IgE-/- animals that are incapable of producing IgE in response to A. fumigatus. The recruitment of eosinophils to the airways was also reduced in IgE-/- mice. Analyses of potential cellular targets of IgE revealed that IgE Abs are not required for the induction of mast cell progenitors in response to allergen, but rather act by sustaining the survival of mature mast cells. Our results identify an important role for IgE Abs in promoting mast cell expansion during allergic responses in vivo.
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U2 - 10.4049/jimmunol.0801569
DO - 10.4049/jimmunol.0801569
M3 - Article
VL - 182
SP - 2416
EP - 2424
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 4
ER -