University of Dundee

MRS studentship - Immune mediators which cause lung fibrosis

The closing date for applications is Friday 12th February 2021

This project is one of 19 four year PhD Studentships funded by Medical Research Scotland ( to be delivered jointly by the named University and External Partner Organisation (EPO). The Studentship will provide the first-class academic and additional training provided by the EPO needed to equip the successful candidate for a science career in an increasingly competitive market.

"Immune mediators which cause lung fibrosis - Halting pulmonary fibrosis through interference in the IL-25, IL-33 and TSLP pathways" to be delivered by the University of Dundee [Supervisors: Dr Henry McSorley and Professor Simon Arthur (both Cell Signalling and Immunology, School of Life Sciences, University of Dundee)] and AstraZeneca UK Limited ( [External Partner Organisation supervisor: Dr E Suzanne Cohen].

Idiopathic pulmonary fibrosis (IPF) is a serious lung disease, which kills around 5000 people a year in the UK. This project aims to understand the signals that lead to IPF, and how these could be better controlled.

IPF is caused by lung scarring (fibrosis), resulting in reduced lung function. The signals which lead to lung damage and scarring are not well understood, but the immune system is clearly involved. In allergic lung conditions such as asthma, an allergic immune response causes damage and inflammation in the lung: in IPF, similar types of immune responses appear to cause aberrant healing of tissue.

The lung tissue communicates with the immune system through the release of "messenger" molecules - cytokines - from the epithelium of the lung. Epithelial cytokines with particularly importance in asthma are IL-25, IL-33 and TSLP. These molecules induce allergic asthma, and clinical trials are underway to block these molecules to attempt to reduce disease. However, recent evidence indicates that IL-25, IL-33 and TSLP work together, and that full suppression of immune responses only occurs when all three of these molecules are blocked simultaneously. We hypothesise that the same is true in fibrosis.

Parasitic worms are particularly good at suppressing allergic immune responses, allowing them to survive in their hosts. We have shown that parasitic worms can suppress these epithelial cytokine responses (especially IL-33) through uniquely effective pathways, avoiding tissue scarring. We will use parasite products and/or blocking proteins to suppress IL-25, IL-33 and TSLP, to treat IPF.


Enquiries should be sent by email to Dr Henry McSorley:


Applicants must have obtained, or expect to obtain, a first or 2.1 UK honours degree, or equivalent for degrees obtained outside the UK, in an appropriate discipline.

Applicants should follow the directions at

and send a CV, the contact details of 2 or 3 referees (including email addresses) and a covering letter, explaining why you have chosen to apply for this particular project, by email to Dr Henry McSorley:

Please note, your application may be shared with the funders of this PhD Studentship, Medical Research Scotland and AstraZeneca UK Ltd.

Interviews are expected to take place 3-4 weeks after the closing date for applications. In light of the current coronavirus situation, interviews may be conducted by video conference.

It is anticipated that the PhD Studentship will start 1 October 2021.

Funding Notes

PhD Studentship provides: an annual tax-free stipend of £18,500, increasing to £19,000 over the four years; tuition fees at UK rates only; consumables; and generous travel allowance. Please note : Applications can only be accepted from UK applicants for this studentship.