{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T06:34:53Z","timestamp":1791182093764,"version":"4.1.0"},"reference-count":27,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2006,9,1]],"date-time":"2006-09-01T00:00:00Z","timestamp":1157068800000},"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":[[2006,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Reactive mastocytosis (RM) in epithelial surfaces is a consistent Th2-associated feature of allergic disease. RM fails to develop in mice lacking leukotriene (LT) C4 synthase (LTC4S), which is required for cysteinyl leukotriene (cys-LT) production. We now report that IL-4, which induces LTC4S expression by mast cells (MCs), requires cys-LTs, the cys-LT type 1 receptor (CysLT1), and Gi proteins to promote MC proliferation. LTD4 (10\u20131000 nM) enhanced proliferation of human MCs in a CysLT1-dependent, pertussis toxin-sensitive manner. LTD4-induced phosphorylation of ERK required transactivation of c-kit. IL-4-driven comitogenesis was likewise sensitive to pertussis toxin or a CysLT1-selective antagonist and was attenuated by treatment with leukotriene synthesis inhibitors. Mouse MCs lacking LTC4S or CysLT1 showed substantially diminished IL-4-induced comitogenesis. Thus, IL-4 induces proliferation in part by inducing LTC4S and cys-LT generation, which causes CysLT1 to transactivate c-kit in RM.<\/jats:p>","DOI":"10.4049\/jimmunol.177.5.2755","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:38:50Z","timestamp":1397849930000},"page":"2755-2759","source":"Crossref","is-referenced-by-count":57,"title":["Cutting Edge: Interleukin 4-Dependent Mast Cell Proliferation Requires Autocrine\/Intracrine Cysteinyl Leukotriene-Induced Signaling"],"prefix":"10.1093","volume":"177","author":[{"given":"Yongfeng","family":"Jiang","sequence":"first","affiliation":[{"name":"Departments of Medicine and Pediatrics, Harvard Medical School , Boston, MA 02115"},{"name":"Division of Rheumatology, Immunology, and Allergy, Brigham and Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshihide","family":"Kanaoka","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Pediatrics, Harvard Medical School , Boston, MA 02115"},{"name":"Division of Rheumatology, Immunology, and Allergy, Brigham and Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chunl","family":"Feng","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Immunology, and Allergy, Brigham and Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karl","family":"Nocka","sequence":"additional","affiliation":[{"name":"UCB Pharma , Cambridge, MA 02140"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sudhir","family":"Rao","sequence":"additional","affiliation":[{"name":"UCB Pharma , Cambridge, MA 02140"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua A","family":"Boyce","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Pediatrics, Harvard Medical School , Boston, MA 02115"},{"name":"Division of Rheumatology, Immunology, and Allergy, Brigham and Women\u2019s Hospital , Boston, MA 02115"},{"name":"Partners Asthma Center , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,9,1]]},"reference":[{"key":"2026020209060116900_R1","first-page":"24","volume-title":"J. 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