{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T08:46:29Z","timestamp":1770108389662,"version":"3.49.0"},"reference-count":52,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2004,1,1]],"date-time":"2004-01-01T00:00:00Z","timestamp":1072915200000},"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":[[2004,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The development of airways hyperreactivity in allergic IL-13\u2212\/\u2212 mice is controversial and appears to correlate with the number of times that the original 129 \u00d7 C57BL\/6 founder strain has been crossed to the BALB\/c background. In this investigation, we compared allergic responses in founder IL-13\u2212\/\u2212 mice crossed for either 5 (N5) or 10 (N10) generations to BALB\/c mice. Whereas allergic N5 IL-13\u2212\/\u2212 mice developed airways hyperreactivity, tissue eosinophilia, elevated IgE, and pulmonary expression of Ym proteins, these processes were attenuated in N5 IL-13\u2212\/\u2212 mice treated with an IL-4-neutralizing Ab, and in N10 IL-13\u2212\/\u2212 mice. These data showed that IL-4 was more effective in regulating allergic responses in N5 IL-13\u2212\/\u2212 mice than in N10 IL-13\u2212\/\u2212 mice. To elucidate the mechanism associated with these observations, we show by restriction and sequence analysis that N5 IL-13\u2212\/\u2212 mice express the C57BL\/6 form of IL-4R\u03b1 and N10 IL-13\u2212\/\u2212 mice express the BALB\/c form. Despite the near identical predicted molecular mass of these isoforms, IL-4R\u03b1 from N5 IL-13\u2212\/\u2212 mice migrates with a slower electrophoretic mobility than IL-4R\u03b1 from N10 IL-13\u2212\/\u2212 mice, suggesting more extensive posttranslational modification of the N5 form. The Thre49Ile polymorphism in the extracellular domain of BALB\/c IL-4R\u03b1 has been demonstrated to disrupt N-linked glycosylation of Asn47 and increase the dissociation rate of the IL-4R\u03b1\/IL-4 interaction. Collectively, these data show that polymorphisms in IL-4R\u03b1, which have been shown to affect the interaction with IL-4, correlate with the ability of IL-4 to regulate allergic responses in IL-13\u2212\/\u2212 mice.<\/jats:p>","DOI":"10.4049\/jimmunol.172.2.1092","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:30:46Z","timestamp":1398025846000},"page":"1092-1098","source":"Crossref","is-referenced-by-count":20,"title":["Polymorphisms in IL-4R\u03b1 Correlate with Airways Hyperreactivity, Eosinophilia, and Ym Protein Expression in Allergic IL-13\u2212\/\u2212 Mice"],"prefix":"10.1093","volume":"172","author":[{"given":"Dianne C","family":"Webb","sequence":"first","affiliation":[{"name":"Division of Molecular Bioscience, The John Curtin School of Medical Research, Australian National University , Australian Capital Territory ,","place":["Australia"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Klaus I","family":"Matthaei","sequence":"additional","affiliation":[{"name":"Division of Molecular Bioscience, The John Curtin School of Medical Research, Australian National University , Australian Capital Territory ,","place":["Australia"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yeping","family":"Cai","sequence":"additional","affiliation":[{"name":"Division of Molecular Bioscience, The John Curtin School of Medical Research, Australian National University , Australian Capital Territory ,","place":["Australia"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew N J","family":"McKenzie","sequence":"additional","affiliation":[{"name":"Medical Research Council Laboratory of Molecular Biology , Cambridge ,","place":["United Kingdom"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul S","family":"Foster","sequence":"additional","affiliation":[{"name":"Division of Molecular Bioscience, The John Curtin School of Medical Research, Australian National University , Australian Capital Territory ,","place":["Australia"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2004,1,15]]},"reference":[{"key":"2026020214134060000_R1","first-page":"109","volume-title":"Am. 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