{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T23:19:46Z","timestamp":1788477586895,"version":"build-2803163510"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2005,7,1]],"date-time":"2005-07-01T00:00:00Z","timestamp":1120176000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Anaphylaxis represents an extreme form of allergic reaction, consisting of a sensitization phase during which allergen-specific IgE are produced and an acute effector phase triggered by allergen-induced degranulation of mast cells. We studied the role of IL-9, a Th2 cytokine implicated in asthma, in different models of murine anaphylaxis. Using a passive model of systemic anaphylaxis, in which anti-DNP IgE Abs were administered before challenge with DNP-BSA, we found that IL-9-transgenic mice or wild-type mice treated with IL-9 for 5 days were highly sensitive to fatal anaphylaxis. This effect was reproduced in both anaphylaxis-susceptible and -resistant backgrounds (FVB\/N or [FVB\/N \u00d7 BALB\/c] F1 mice, respectively) and correlated with increased serum concentrations of mouse mast cell protease-1 level, a protein released upon mast cells degranulation. By contrast, IL-9 did not increase the susceptibility to passive cutaneous anaphylaxis. IL-9 expression also increased the susceptibility to fatal anaphylaxis when mice were sensitized by immunization against OVA before challenge with the same Ag. In this model, serum from sensitized, IL-9-transgenic mice was more potent in transferring susceptibility to OVA challenge into naive mice, indicating that IL-9 also promotes the sensitization stage. Finally, using IL-9R-deficient mice, we found that despite its anaphylaxis-promoting activity, IL-9 is dispensable for development of both passive and active anaphylaxis, at least in the C57BL\/6 mouse background. Taken together, the data reported in this study indicate that IL-9 promotes systemic anaphylaxis reactions, acting at both the sensitization and effector stages, but is not absolutely required for this process.<\/jats:p>","DOI":"10.4049\/jimmunol.175.1.335","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T01:08:21Z","timestamp":1398042501000},"page":"335-341","source":"Crossref","is-referenced-by-count":30,"title":["IL-9 Promotes but Is Not Necessary for Systemic Anaphylaxis"],"prefix":"10.1093","volume":"175","author":[{"given":"Laurent","family":"Knoops","sequence":"first","affiliation":[{"name":"Ludwig Institute for Cancer Research, Brussels Branch, and Experimental Medicine Unit, Universite\u0301 de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamila","family":"Louahed","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research, Brussels Branch, and Experimental Medicine Unit, Universite\u0301 de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Van Snick","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research, Brussels Branch, and Experimental Medicine Unit, Universite\u0301 de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Christophe","family":"Renauld","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research, Brussels Branch, and Experimental Medicine Unit, Universite\u0301 de Louvain , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2005,7,1]]},"reference":[{"key":"2025032808273265700_R1","first-page":"S53","volume-title":"J. 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