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Background <p>Evidence demonstrates that megakaryocytes (MKs) possess antigen processing and presentation properties. We investigated whether sensitisation to house dust mite (HDM) extract and the establishment of allergic pulmonary inflammation was dependent on the presence of platelets, and whether the allergic phenotype had an effect on antigen-presenting marker expression on MKs and platelets.</p> Methods <p>Balb/c mice were administered anti-GPIbα antibody or an isotype control during days 0, 2, and 4 to temporarily deplete circulating platelets during initial sensitization to allergen (HDM extract) via an extended intranasal administration on days 0–4, 7–11, and 13. Bronchoalveolar lavage was undertaken, along with blood samples, and lung histology to quantify leukocyte recruitment, Th2 cytokine analysis, and lung platelet deposition. Lung MKs, bone marrow MKs, and circulating platelets were analysed from both allergen-sensitized and non-sensitized mice for the expression of MHC class I, MHC class II, FcεRIα, and CD40.</p> Results <p>Temporary platelet depletion limited to the initial phase of allergen sensitization inhibited the development of the allergic pulmonary phenotype to HDM as demonstrated by reduced eosinophil recruitment, IgE titre, IL-4 and IL-13 expression. Lung-resident MKs demonstrated higher expression of MHC class II and FcεRIα when compared to bone marrow (BM) MKs on establishment of an allergic phenotype, suggesting the administration of HDM specifically affected the immune-phenotype of the lung niche of MKs rather than the bone marrow niche, or systemic effects on circulating platelets. Platelets within the lung were observed to have increased co-localisation frequency with CD11c-positive antigen-presenting cells (APCs), but not CD4-positive T cells, suggesting that platelet activation may occur during the initial steps of allergen sensitisation.</p> Conclusion <p>The platelet/MK axis is a requirement for sensitisation to HDM. An allergic phenotype selectively influences the immune signature of MKs in the lung.</p>

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The Platelet/Megakaryocyte Axis is Necessary for Allergic Sensitisation and Inflammatory Responses to House Dust Mite in the Lung

  • 期刊论文

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  • 发表日期：

    2026年5月19日

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  • Anna Chalidou,
  • Katie-Marie Case,
  • Carl Hobbs,
  • Clive P. Page,
  • Simon C. Pitchford

摘要

Background

Evidence demonstrates that megakaryocytes (MKs) possess antigen processing and presentation properties. We investigated whether sensitisation to house dust mite (HDM) extract and the establishment of allergic pulmonary inflammation was dependent on the presence of platelets, and whether the allergic phenotype had an effect on antigen-presenting marker expression on MKs and platelets.

Methods

Balb/c mice were administered anti-GPIbα antibody or an isotype control during days 0, 2, and 4 to temporarily deplete circulating platelets during initial sensitization to allergen (HDM extract) via an extended intranasal administration on days 0–4, 7–11, and 13. Bronchoalveolar lavage was undertaken, along with blood samples, and lung histology to quantify leukocyte recruitment, Th2 cytokine analysis, and lung platelet deposition. Lung MKs, bone marrow MKs, and circulating platelets were analysed from both allergen-sensitized and non-sensitized mice for the expression of MHC class I, MHC class II, FcεRIα, and CD40.

Results

Temporary platelet depletion limited to the initial phase of allergen sensitization inhibited the development of the allergic pulmonary phenotype to HDM as demonstrated by reduced eosinophil recruitment, IgE titre, IL-4 and IL-13 expression. Lung-resident MKs demonstrated higher expression of MHC class II and FcεRIα when compared to bone marrow (BM) MKs on establishment of an allergic phenotype, suggesting the administration of HDM specifically affected the immune-phenotype of the lung niche of MKs rather than the bone marrow niche, or systemic effects on circulating platelets. Platelets within the lung were observed to have increased co-localisation frequency with CD11c-positive antigen-presenting cells (APCs), but not CD4-positive T cells, suggesting that platelet activation may occur during the initial steps of allergen sensitisation.

Conclusion

The platelet/MK axis is a requirement for sensitisation to HDM. An allergic phenotype selectively influences the immune signature of MKs in the lung.