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UK-Förderung (135.507 £): Studie zu den potenziell therapeutischen immunmodulatorischen Wirkungen von gp120 bei rheumatischen Autoimmunerkrankungen Ukri 04.12.2014 Forschung und Innovation im Vereinigten Königreich, Großbritannien
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Studie zu den potenziell therapeutischen immunmodulatorischen Wirkungen von gp120 bei rheumatischen Autoimmunerkrankungen
| Zusammenfassung | This project focuses on two devastating diseases called Rheumatoid Arthritis (RA) and Systemic Lupus Erythematous (SLE). These are autoimmune diseases where instead of the immune system only fighting infection, it becomes over activated and causes inflammation which is damaging to the body. In RA this mainly affects the lining of the joints, whereas in SLE it can affect lots of parts of the body including the joints, the skin, the lungs, kidney and brain. These diseases can be life-threatening but treatment so far has focused on dampening down the immune system to control and limit the damage caused by the inflammation. These treatments often have side effects, particularly leading to severe infections, or do not work in all people. As medical science progresses we learn more about what causes these diseases and so we can focus on developing so-called targeted treatments to stop them. Not all immune diseases cause inflammation however. In Human Immunodeficiency Virus (HIV) infection the virus can change the immune system's balance towards an anti-inflammatory state. Although this helps HIV spread, it can also teach us lessons and suggest ideas to suppress the immune system in a targeted way. HIV has a protein on its surface called gp120, and it is this protein that interacts with elements of the immune system, leading to targeted suppression. Taken away from the virus and by itself this protein is not infective and is not dangerous. However, research shows that gp120 by itself has a number of interesting effects that together decrease immune activation and dampen down inflammation. In inflammation, cells can produce products called cytokines that drive the cycle of inflammation further. One such example is interferon-alpha (IFNa) which is mainly produced by a cell subtype called plasmacytoid dendritic cells (pDCs). IFNa has been shown to be damaging in RA and in SLE. Interestingly however, gp120 can reduce pDCs from making these damaging inflammatory cytokines, including IFNa. In pDCs gp120 can also increase levels of an enzyme called IDO. This is an important enzyme as it works to reduce inflammation. It does this by both increasing the number of anti-inflammatory immune cells and also reducing the number of inflammatory immune cells. Finally pDCs that have been treated with gp120 can affect other cells (B-cells) to reduce the levels of autoantibodies in the blood. Autoantibodies are markers of autoimmune disease and are seen in RA and SLE. In this project I want to find out more about what part pDCs play in RA and SLE disease. I also want to see if gp120 can help to reduce any damaging actions of pDCs in these diseases. If this worked, gp120 could be developed as a new treatment for RA and SLE. I will research this by firstly looking at what the gp120 does on pDCs and other cell types taken from the blood of healthy volunteers. I will next see what happens when using blood from patients with RA and SLE. In patients with RA I will also look at pDCs taken from synovial fluid and synovium (this is the lining of the joint and the fluid that surrounds it) which becomes damaged in RA. By carrying out the above research I believe that I can 1) start to answer the question if gp120 can be developed as a new treatment for RA and SLE as well as 2) add to the knowledge about what role pDCs have in RA and SLE. |
| Kategorie | Fellowship |
| Referenz | MR/M003183/1 |
| Status | Closed |
| Laufzeit von | 04.12.2014 |
| Laufzeit bis | 03.12.2016 |
| Fördersumme | 135.507,00 £ |
| Quelle | https://gtr.ukri.org/projects?ref=MR%2FM003183%2F1 |
Beteiligte Organisationen
| NEWCASTLE UNIVERSITY | |
| Pasteur Institute, Paris |
Die Bekanntmachung bezieht sich auf einen vergangenen Zeitpunkt, und spiegelt nicht notwendigerweise den heutigen Stand wider. Der letzte verfügbare Stand wird auf folgender Seite wiedergegeben: Newcastle University, Newcastle Upon Tyne, Großbritannien.