Supplementary Materials

Supplementary Material for:

TH2 and TH17 inflammatory pathways are reciprocally regulated in asthma

David F. Choy, Kevin M. Hart, Lee A. Borthwick, Aarti Shikotra, Deepti R. Nagarkar, Salman Siddiqui, Guiquan Jia, Chandra M. Ohri, Emma Doran, Kevin M. Vannella, Claire A. Butler, Beverley Hargadon, Joshua C. Sciurba, Richard L. Gieseck, Robert W. Thompson, Sandra White, Alexander R. Abbas, Janet Jackman, Lawren C. Wu, Jackson G. Egen, Liam G. Heaney, Thirumalai R. Ramalingam, Joseph R. Arron,* Thomas A. Wynn, Peter Bradding

*Corresponding author. E-mail: arron.joseph{at}gene.com

Published 19 August 2015, Sci. Transl. Med. 7, 301ra129 (2015)
DOI: 10.1126/scitranslmed.aab3142

This PDF file includes:

  • Fig. S1. Intercorrelation between the three IL-13–inducible genes and the five IL-17–inducible genes in endobronchial biopsies.
  • Fig. S2. Neutrophilic inflammation in peripheral or airway compartments is not associated with molecular phenotypes of TH2 or TH17 inflammation.
  • Fig. S3. Differential effects of TH2 blockade on mucous and inflammatory responses in allergic asthma.
  • Fig. S4. Dexamethasone suppresses TH2 pathways but enhances TH17 pathways in the mouse asthma model.
  • Fig. S5. Evidence of dual cross-regulation between the TH2 and TH17 cytokine networks.
  • Fig. S6. A summary of the potential interplay between TH2 (IL-4/13)– and IL-17–dependent signaling in asthmatic airways.
  • Table S1. Mutual exclusivity of IL-17 and IL-13 expression in endobronchial biopsies.
  • Table S2. Clinical characteristics of TH2/17-low, TH2-high, and TH17-high asthma.

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