How do certain types of immune cell protect against joint inflammation in rheumatoid arthritis?
Disease - Rheumatoid Arthritis
Lead applicant - Dr Mariola Kurowska-Stolarska
Organisation - University of Glasgow
Type of grant - Full Application Disease
Status of grant - Pending Start Date
Amount of the original award - £442,659.00
Start date - 14 July 2020
Reference - 22272
Public Summary
What are the aims of this research?
There are a variety of treatments available for rheumatoid arthritis, but less than half of patients go into remission and even less patients stay in long-term drug-free remission. The mechanisms that keep joints in remission (free of inflammation) in rheumatoid arthritis are not well under-stood. This research will investigate how a group of ‘protective’ macrophages (white blood cells involved in many inflammatory diseases) may help to prevent inflammation and maintain joint re-mission in rheumatoid arthritis. The researchers will explore how these macrophage cells interact with other cells in the joint, and how they affect inflammation.
Why is this research important?
Whilst many people with rheumatoid arthritis respond well to treatment, few people are free from inflammation. Previous research has found a type of macrophage in rheumatoid arthritis patients who are in remission, that is not present in patients who did not go into remission. Analysis of these macrophage cells suggests they might actively protect the joints from recurrence of inflammation. During this project, researchers will isolate the ‘protective’ macrophages from joint samples of rheumatoid arthritis patients in remission and explore how they influence the structure and integrity of the joint. Researchers will also study which molecules stimulate or block the activation of these ‘protective’ macrophages in order to prevent inflammation.
How will the findings benefit patients?
This research will improve our understanding of cells that protect against inflammation in rheumatoid arthritis and the biological mechanisms that drive these cells. This knowledge may direct the development of new drugs that encourage the activation, development or replacement of these cells in order to resolve inflammation and maintain joint remission.