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John L. Dart Library
9 a.m. - 5 p.m.
Phone: (843) 722-7550
West Ashley Library
9 a.m. - 5 p.m.
Phone: (843) 766-6635
Folly Beach Library
9 a.m. - 2 p.m.
*open the 2nd and 4th Saturday
*open the 2nd and 4th Saturday
Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
Wando Mount Pleasant Library
9 a.m. - 5 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. - 1 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. - 5 p.m.
Phone: (843) 889-3300
Otranto Road Library
9 a.m. - 5 p.m.
Phone: (843) 572-4094
Mt. Pleasant Library
9 a.m. – 5 p.m.
Phone: (843) 849-6161
McClellanville Library
9 a.m. – 1 p.m.
Phone: (843) 887-3699
Keith Summey North Charleston Library
9 a.m. - 5 p.m.
Phone: (843) 744-2489
John's Island Library
9 a.m. - 5 p.m.
Phone: (843) 559-1945
Hurd/St. Andrews Library
9 a.m. - 5 p.m.
Phone: (843) 766-2546
Miss Jane's Building (Edisto Library Temporary Location)
9 a.m. – 1 p.m.
Phone: (843) 869-2355
Dorchester Road Library
9 a.m. - 5 p.m.
Phone: (843) 552-6466
Baxter-Patrick James Island
9 a.m. - 5 p.m.
Phone: (843) 795-6679
Main Library
9 a.m. - 5 p.m.
Phone: (843) 805-6930
Bees Ferry West Ashley Library
9 a.m. - 5 p.m.
Phone: (843) 805-6892
Mobile Library
Closed
Phone: (843) 805-6909
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Involvement of the epidermal growth factor receptor in IL‐13–mediated corticosteroid‐resistant airway inflammation.
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- Author(s): Davies, Elizabeth R. (AUTHOR); Perotin, Jeanne‐Marie (AUTHOR); Kelly, Joanne F.C. (AUTHOR); Djukanovic, Ratko (AUTHOR); Davies, Donna E. (AUTHOR); Haitchi, Hans Michael (AUTHOR)
- Source:
Clinical & Experimental Allergy. Jun2020, Vol. 50 Issue 6, p672-686. 15p. 1 Color Photograph, 1 Chart, 7 Graphs. - Source:
- Additional Information
- Subject Terms:
- Abstract: Background: Effective treatment for severe asthma is a significant unmet need. While eosinophilic inflammation caused by type 2 cytokines is responsive to corticosteroid and biologic therapies, many severe asthmatics exhibit corticosteroid‐unresponsive mixed granulocytic inflammation. Objective: Here, we tested the hypothesis that the pro‐allergic cytokine, IL‐13, can drive both corticosteroid‐sensitive and corticosteroid‐resistant responses. Results: By integration of in vivo and in vitro models of IL‐13–driven inflammation, we identify a role for the epidermal growth factor receptor (EGFR/ERBB1) as a mediator of corticosteroid‐unresponsive inflammation and bronchial hyperresponsiveness driven by IL‐13. Topological data analysis using human epithelial transcriptomic data from the U‐BIOPRED cohort identified severe asthma groups with features consistent with the presence of IL‐13 and EGFR/ERBB activation, with involvement of distinct EGFR ligands. Our data suggest that IL–13 may play a dual role in severe asthma: on the one hand driving pathologic corticosteroid‐refractory mixed granulocytic inflammation, but on the other hand underpinning beneficial epithelial repair responses, which may confound responses in clinical trials. Conclusion and Clinical Relevance: Detailed dissection of those molecular pathways that are downstream of IL‐13 and utilize the ERBB receptor and ligand family to drive corticosteroid‐refractory inflammation should enhance the development of new treatments that target this sub‐phenotype(s) of severe asthma, where there is an unmet need. [ABSTRACT FROM AUTHOR]
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