Polymorphisms in IL-4Rα Correlate with Airways Hyperreactivity, Eosinophilia, and Ym Protein Expression in Allergic IL-13-/- Mice

Dianne C. Webb*, Klaus I. Matthaei, Yeping Cai, Andrew N.J. McKenzie, Paul S. Foster

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    31 Citations (Scopus)

    Abstract

    The development of airways hyperreactivity in allergic IL-13-/- mice is controversial and appears to correlate with the number of times that the original 129 × C57BL/6 founder strain has been crossed to the BALB/c background. In this investigation, we compared allergic responses in founder IL-13-/- mice crossed for either 5 (N5) or 10 (N10) generations to BALB/c mice. Whereas allergic N5 IL-13-/- mice developed airways hyperreactivity, tissue eosinophilia, elevated IgE, and pulmonary expression of Ym proteins, these processes were attenuated in N5 IL-13-/- mice treated with an IL-4-neutralizing Ab, and in N10 IL-13-/- mice. These data showed that IL-4 was more effective in regulating allergic responses in N5 IL-13-/- mice than in N10 IL-13-/- mice. To elucidate the mechanism associated with these observations, we show by restriction and sequence analysis that N5 IL-13-/- mice express the C57BL/6 form of IL-4Rα and N10 IL-13-/- mice express the BALB/ c form. Despite the near identical predicted molecular mass of these isoforms, IL-4Rα from N5 IL-13-/- mice migrates with a slower electrophoretic mobility than IL-4Rα from N10 IL-13-/- mice, suggesting more extensive posttranslational modification of the N5 form. The Thre49 Ile polymorphism in the extracellular domain of BALB/c IL-4Rα has been demonstrated to disrupt N-linked glycosylation of Asn 47 and increase the dissociation rate of the IL-4Rα/IL-4 interaction. Collectively, these data show that polymorphisms in IL-4Rα, 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-/- mice.

    Original languageEnglish
    Pages (from-to)1092-1098
    Number of pages7
    JournalJournal of Immunology
    Volume172
    Issue number2
    DOIs
    Publication statusPublished - 15 Jan 2004

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