The role of fibroblasts in giant cell arteritis

  • Research type

    Research Study

  • Full title

    Unravelling the role of fibroblasts in giant cell arteritis and establishing their contribution in the promotion of inflammation and disease relapse.

  • IRAS ID

    309672

  • Contact name

    Maira Karabayas

  • Contact email

    maira.karabayas@abdn.ac.uk

  • Sponsor organisation

    University of Aberdeen

  • Duration of Study in the UK

    3 years, 11 months, 30 days

  • Research summary

    Giant cell arteritis (GCA) is a common inflammatory disease of old-age that affects the large arteries of the body, and primarily the arteries supplying the head. Patients commonly experience musculoskeletal pain, fatigue, visual disturbances and jaw pain. Untreated, patients can suffer blindness, stroke or sudden death. Historically, steroids have been the mainstay of treatment. While these can reduce these disease complications in the short-term, they are associated with significant side-effects, including serious infections causing hospitalisations, osteoporosis and fractures, high blood pressure and diabetes. Additional drugs can be used to partially spare this burden. However, options are limited and despite inflammation persists in many patients, reflected by the frequent return of the disease and debilitating symptoms. Thus, there is an unmet need to understand the biological mechanisms that sustain this disease state.

    This study seeks to investigate the cells within the arterial wall which interact with resident cells and cells of the immune system and test if they behave as orchestrators of inflammation responsible for relapsing symptoms. The cells of particular interest are fibroblasts. Fibroblasts have been shown in other diseases such as rheumatoid arthritis to play a pivotal role in mediating inflammation.

    To deliver this, first I will use artery tissue, which has been previously collected from patients presenting with GCA (supplied via the NHSG biorepository), to map the distribution of fibroblasts Second, I will collect fresh artery and blood samples from relapsing patients and I will apply state of the art laboratory technologies to evaluate their function and importance. I will then interrogate their interactions with immune cells to ascertain the mechanisms by which they promote persistence of inflammation and drive relapse.

    Understanding the contribution of fibroblasts on persistent inflammation might allow for the development of new targeted drugs that can alleviate this disease state and ultimately lead to better outcomes and quality of life for patients with GCA.

  • REC name

    North of Scotland Research Ethics Committee 2

  • REC reference

    22/NS/0001

  • Date of REC Opinion

    3 Feb 2022

  • REC opinion

    Further Information Favourable Opinion