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Epithelial signatures in respiratory disease


Please use this identifier to cite or link to this item: http://hdl.handle.net/2077/69673

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Title: Epithelial signatures in respiratory disease
Authors: Ax, Elisabeth
Issue Date: 25-Nov-2021
University: University of Gothenburg. Sahlgrenska Academy
Institution: Inst of Medicine. Department of Internal Medicine and Clinical Nutrition
Parts of work: I. Jevnikar, Z., Östling, J., Ax, E., Calvén, J., Thörn, K., Israelsson, E., Öberg, L., Singhania, A., Lau, L.C.K., Wilson, S..J, Ward, J.A., Chauhan, A., Sousa, A.R., De Meulder, B., Loza, M.J., Baribaud, F., Sterk, P.J., Chung, K.F., Sun, K., Guo, Y., Adcock, I.M., Payne, D., Dahlén, B., Chanez, P., Shaw, D.E., Krug, N., Hohlfeld, J.M., Sandström, T., Djukanovic, R., James, A., Hinks, T.S.C., Howarth, P.H., Vaarala, O., van Geest, M. & Olsson, H.; Unbiased Biomarkers in Prediction of Respiratory Disease Outcomes study group. (2019). Epithelial IL-6 trans-signaling defines a new asthma phenotype with increased airway inflammation. Journal of Allergy and Clinical Immunology, 143(2), 577-590.
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II. Ax, E., Jevnikar, Z., Cvjetkovic, A., Malmhäll, C., Olsson, H., Rådinger, M. & Lässer, C. (2020). T2 and T17 cytokines alter the cargo and function of airway epithelium-derived extracellular vesicles. Respiratory Research, 21:155.
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III. Ax, E., Weidner, J., Winslow, S., Lässer, C., Jevnikar, Z., Olsson, H. & Rådinger, M., Th17 cytokines mediate airway epithelial barrier dysfunction – A possible role for miRNAs. In manuscript.
Date of Defence: 2021-12-16
Disputation: Torsdagen den 16 december 2021, kl. 9.00, Hörsal Europa, Konferenscentrum Wallenberg, Medicinaregatan 20, Göteborg
Degree: Doctor of Philosophy (Medicine)
Publication type: Doctoral thesis
Keywords: airway epithelium
inflammation
gene expression
extracellular vesicles
miRNA
Abstract: The epithelium of the human airways protects us against harm and helps maintain immune homeostasis. In respiratory diseases such as asthma and COPD, the functions of the epithelium are altered and can cause or contribute to disease progression. Additionally, these diseases are heterogeneous in regard to which inflammatory mechanisms and pathways are activated, thus creating inflammatory endotypes. Due to these differing endotypes, not all patients respond similarly to currently available t... more
ISBN: 978-91-8009-552-5 (PRINT)
978-91-8009-553-2 (PDF)
URI: http://hdl.handle.net/2077/69673
Appears in Collections:Doctoral Theses from Sahlgrenska Academy
Doctoral Theses from University of Gothenburg / Doktorsavhandlingar från Göteborgs universitet
Doctoral Theses / Doktorsavhandlingar Institutionen för medicin

 

 

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