Siglec-F-dependent negative regulation of allergen-induced eosinophilia depends critically on the experimental model

Sarah J. McMillan, Hannah E. Richards, Paul R. Crocker (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    19 Citations (Scopus)
    204 Downloads (Pure)


    Siglec-8 and siglec-F are paralogous membrane proteins expressed on human and murine eosinophils respectively. They bind similar sialylated and sulphated glycans and mediate eosinophil apoptosis when cross-linked with antibodies or glycan ligands. In models of allergic eosinophilic airway inflammation, siglec-F was shown previously to be important for negatively regulating eosinophilia. It was proposed that this was due to siglec-F-dependent apoptosis, triggered via engagement with ligands that are upregulated on bronchial epithelium. Our aim was to further investigate the functions of siglec-F by comparing two commonly used models of ovalbumin-induced airway inflammation that differ in the dose and route of administration of ovalbumin. In confirmation of published results, siglec-F-deficient mice had enhanced lung tissue eosinophilia in response to intranasal ovalbumin delivered every other day. However, following aerosolised ovalbumin delivered daily, there was no influence of siglec-F deficiency on lung eosinophilia. Expression of siglec-F ligands in lung tissues was similar in both models of allergen induced inflammation. These data demonstrate that siglec-F-dependent regulation of eosinophilia is subtle and depends critically on the model used. The findings also indicate that mechanisms other than ligand-induced apoptosis may be important in siglec-F-dependent suppression of eosinophilia.
    Original languageEnglish
    Pages (from-to)11-16
    Number of pages6
    JournalImmunology Letters
    Issue number1
    Publication statusPublished - 2014


    Dive into the research topics of 'Siglec-F-dependent negative regulation of allergen-induced eosinophilia depends critically on the experimental model'. Together they form a unique fingerprint.

    Cite this