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Project description


Rheumatoid arthritis (RA) is destructive autoimmune joint disease. The recent development of new drugs has improved the disease outcome. Unfortunately, the side-effects of therapy, the RA itself, and the implantation of prosthetic joints render patients sensitive to bacterial joint infections. The most common agent causing joint infections is Staphylococcus aureus, which can cause sepsis and septic arthritis. S. aureus-induced arthritis is a severe problem with high mortality and morbidity rates. Thus, there is a need for new effective RA treatment modalities that do not increase sensitivity to infections and new ways to treat S. aureus infection that reduce both the associated mortality and morbidity.

A tempting approach to develop new drugs against RA is to induce immune tolerance. This could be achieved by manipulating the immune system, so that the immune attack against the host’s own tissue (e.g. joints) is abolished. We target the expression of specific proteins (e.g. self-antigens and/or cytokines) using self-inactivating lentiviral vectors in two well-established mouse models of RA: collagen type II (CII)-induced arthritis (CIA) and S. aureus arthritis. We have shown that profylactic treatment using this system significantly improves the outcome of CIA (Mol Ther. 2009 Apr;17(4):632-40). Presently we are investigating if the same system can be used for treatment of a manifest disease and what mechanisms that are involved.

The second part of our project is to increase the knowlegde of immunoregulation during S. aureus arthritis in order to develop new treatment strategies. Presently we study the impact of the interleukins (IL)-10, -17 and IL-15, on the outcome of the disease. Knockout mice and the lentiviral system are together two very useful tools to study the function of these cytokines and their importance for staphylococcal arthritis development and progression.

Inger Gjertsson photo

Kontaktinformation

Inger Gjertsson

Box 480, 405 30 Göteborg

Besöksadress:
Guldhedsgatan 10A

Telefon:
031-342 46 92

Sidansvarig: kommunikation@medicine.gu.se|Sidan uppdaterades: 2017-05-31
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