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 language | English |
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Pages (from-to) | 181-190 |
Number of pages | 10 |
Journal | European Journal of Haematology |
Volume | 77 |
Issue number | 3 |
DOIs | |
Publication status | Published - Sept 2006 |
Externally published | Yes |