Basophils as a primary inducer of the T helper type 2 immunity in ovalbumin-induced allergic airway inflammation

Authors

  • Wenwei Zhong,

    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
    Current affiliation:
    1. Department of Paediatrics, Shanghai Children's Medical Centre Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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    • Wenwei Zhong, Wen Su and Yanjie Zhang contributed equally to this work.
  • Wen Su,

    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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    • Wenwei Zhong, Wen Su and Yanjie Zhang contributed equally to this work.
  • Yanjie Zhang,

    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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    • Wenwei Zhong, Wen Su and Yanjie Zhang contributed equally to this work.
  • Qi Liu,

    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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  • Jinhong Wu,

    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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  • Caixia Di,

    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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  • Zili Zhang,

    1. Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA
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  • Zhenwei Xia

    Corresponding author
    1. Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
    • Correspondence: Dr Zhenwei Xia, Department of Paediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai 200025, China. Email: xzw63@hotmail.com

      Senior author: Zhenwei Xia

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Summary

Antigen-induced allergic airway inflammation is mediated by T helper type 2 (Th2) cells and their cytokines, but the mechanism that initiates the Th2 immunity is not fully understood. Recent studies show that basophils play important roles in initiating Th2 immunity in some inflammatory models. Here we explored the role of basophils in ovalbumin (OVA) -induced airway allergic inflammation in BALB/c mice. We found that OVA sensitization and challenge resulted in a significant increase in the amount of basophils in blood and lung, along with the up-regulation of activation marker of CD200R. However, depletion of basophils with MAR-1 or Ba103 antibody attenuated airway inflammation, represented by the significantly decreased amount of the Th2 subset in spleen and draining lymph nodes, interlukin-4 level in lung and OVA-special immunoglobulin E (sIgE) levels in serum. On the other hand, adoptive transfer of basophils from OVA-challenged lung tissue to naive BALB/c mice provoked the Th2 immune response. In addition, pulmonary basophils from OVA-challenged mice were able to uptake DQ-OVA and express MHC class II molecules and CD40 in vivo, as well as to release interleukin-4 following stimulation by IgE–antigen complexes and promote Th2 polarization in vitro. These findings demonstrate that basophils may participate in Th2 immune responses in antigen-induced allergic airway inflammation and that they do so through facilitating antigen presentation and providing interleukin-4.

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