Interleukin-5 does not influence differential transcription of transmembrane and soluble isoforms of IL-5Rα in vivo

Jonas Byström, Kimberly D. Dyer, Suk See Ting De Ravin, Nora Naumann, David A. Stephany, Paul S. Foster, Thomas A. Wynn, Helene F. Rosenberg*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)

Abstract

Interleukin-5 (IL-5) promotes signal transduction and expansion of eosinophil colonies in bone marrow via interactions with its heterodimeric receptor (IL-5R). Two variants encoding soluble forms of the alpha subunit (sIL-5Rα) have been described, although the signals promoting and/or limiting differential transcription remain to be clarified. Objectives: Our intent was to explore the role of IL-5 in regulating differential transcription of these splice variants in vivo. Methods: We have designed a quantitative reverse transcriptase-polymerase chain reaction assay to detect transcripts encoding the transmembrane, soluble 1 and 2 forms of IL-5Rα in two strains of wild-type (BALB/c and C57BL/6) and corresponding IL-5 gene-deleted mice. Wild-type mice respond to S. mansoni infection with a gradual increase in serum IL-5 and eosinophilia, which is not observed in IL-5 gene-deleted mice. Results and conclusions: We find that IL-5 is not necessary for differential splicing to occur in vivo, as all three forms of the IL-5Rα are detected in both strains of IL-5 gene-deleted mice, with ratios of transcript expression (transmembrane:soluble 1:soluble 2) that were indistinguishable from their wild-type counterparts. Differential splicing does vary markedly between strains, potentially because of local effects of strain-specific polymorphisms.

Original languageEnglish
Pages (from-to)181-190
Number of pages10
JournalEuropean Journal of Haematology
Volume77
Issue number3
DOIs
Publication statusPublished - Sept 2006
Externally publishedYes

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