{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T04:40:36Z","timestamp":1789620036744,"version":"build-2803163510"},"reference-count":41,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2000,3,1]],"date-time":"2000-03-01T00:00:00Z","timestamp":951868800000},"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":[[2000,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Previous studies have suggested that enhancement of mediator release from human basophils by IL-3 occurs in at least two phases, and the current studies further characterize the signaling changes that accompany these two phases of the basophil in response to IL-3. The test stimulus for these studies was anaphylatoxin split product of C component (C5a), which does not induce leukotriene C4 release without prior IL-3 treatment. Functionally, IL-3 priming occurs after 5 min, disappears by 2 h, and returns by 18 h. In contrast, the kinetics of cytosolic phospholipase A2 (cPLA2) and extracellular signal-regulated kinase (ERK1\/2) phosphorylation, induced by IL-3, do not show the second rise by 18 h. The kinetics of cPLA2 and ERK1\/2 phosphorylation following stimulation with C5a are the same for cells that were not treated with IL-3 as for those treated for 18 h, i.e., a lag in phosphorylation of cPLA2 and ERK1\/2 lasting 30 s before its eventual rise. Previous studies showed that a 5-min treatment with IL-3 induced little change in the C5a-induced cytosolic calcium response, while 24 h of treatment resulted in a marked and sustained cytosolic calcium elevation during the C5a-induced response. The first phase of the IL-3 priming effect (5\u201315 min of treatment) was unaffected by cycloheximide, while the second phase (18 h) was inhibited. These data suggest that early IL-3 priming results from preconditioning cPLA2, i.e., causing its phosphorylation, while late priming results from a qualitative change in the cytosolic calcium response.<\/jats:p>","DOI":"10.4049\/jimmunol.164.6.3026","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T20:28:33Z","timestamp":1398198513000},"page":"3026-3034","source":"Crossref","is-referenced-by-count":32,"title":["Dual Phase Priming by IL-3 for Leukotriene C4 Generation in Human Basophils: Difference in Characteristics Between Acute and Late Priming Effects"],"prefix":"10.1093","volume":"164","author":[{"given":"Katsushi","family":"Miura","sequence":"first","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center , Baltimore, MD 21224"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"Donald W","family":"MacGlashan","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center , Baltimore, MD 21224"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,3,15]]},"reference":[{"key":"2025032908420456500_R1","first-page":"2231","volume-title":"J. 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