Supplementary Materials

Supplementary Material for:

Rhinovirus-induced IL-25 in asthma exacerbation drives type 2 immunity and allergic pulmonary inflammation

Janine Beale, Annabelle Jayaraman, David J. Jackson, Jonathan D. R. Macintyre, Michael R. Edwards, Ross P. Walton, Jie Zhu, Yee Man Ching, Betty Shamji, Matt Edwards, John Westwick, David J. Cousins, You Yi Hwang, Andrew McKenzie, Sebastian L. Johnston, Nathan W. Bartlett*

*Corresponding author. E-mail: n.bartlett{at}ic.ac.uk

Published 1 October 2014, Sci. Transl. Med. 6, 256ra134 (2014)
DOI: 10.1126/scitranslmed.3009124

This PDF file includes:

  • Fig. S1. Airway leukocyte infiltration in a model of RV-induced allergic airways disease.
  • Fig. S2. RV infection induces expression by epithelial cells in large airways, bronchioles, and alveoli.
  • Fig. S3. Representative flow plots demonstrating the gating strategy for IL-4+ basophils in whole-lung tissue at day 1 after infection.
  • Fig. S4. Representative flow plots of IL-4+ CD4+ T cells in whole-lung tissue in a model of RV-induced allergic airways disease at day 7 after infection.
  • Fig. S5. Representative flow plots demonstrating the gating strategy for non-T type 2 cells in whole-lung tissue at day 7 after infection.
  • Fig. S6. ICOS+ populations in the lung and mediastinal lymph nodes (MedLN) after allergen challenge.
  • Table S1. Clinical characteristics of volunteers from whom BECs were obtained.
  • Table S2. Summary of correlations between clinical parameters and IL-25 protein levels 24 hours after RV-1B infection or media treatment of cultured BECs from atopic asthmatics (n = 10).
  • Table S3. Baseline demographic and clinical characteristics of volunteers for the human experimental RV infection study.

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