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Etiopathogenesis of reactive arthritis, Reiter's disease and ankylosing spondylitis: Abnormal host - microbe interaction


- To determine microbial structures persisting in reactive arthritis.
- To explore the role of microbes in the etiology and pathogenesis of ankylosing spondylitis.
- To determine defects of HLA B27 positive persons developing reactive arthritis in elimination of causative microbes.
- To determine differences in interaction between reactive arthritis causing microbes and cell lines transfected with HLA B27 and other MHC class I genes.

The chronic nature of HLA B27 associated autoimmune diseases suggests that the antigen triggering and/or maintaining these processes persists in the body, probably inside phagocytic or other cells. This might be due to incomplete function of the elimination system. The proposed research will concentrate on the search and characterization of the antigen(s) triggering and maintaining HLA B27 associated diseases. To study functions of monocyte/ macrophages, fibroblasts, T cells and B cells in the elimination of intestinal pathogens, we take advantage of the participants' expertise in cell biology, immunology, biochemistry and molecular biology. We will also study the mechanisms and molecules which participate in the incomplete elimination of microbial antigens. These molecules include the ones mediating adherence, ingestion, killing and degradation of microbes and adhesion molecules affecting cell-cell and cell-extracellular matrix interactions. The role of HLA B27 is clarified by comparing the function of cells from HLA B27 positive and negative patients and healthy persons, but especially by comparing syngeneic cell lines (monocyte, fibroblast) which differ only in the expression of this important tissue antigen. This approach bypasses the individual variation between persons, which has often made it difficult to draw definite conclusions about the role of HLA B27 in various studies. The final goal of this study is to define the mechanisms leading to the development of HLA B27 associated diseases and eventually develop methods to prevent and treat these handicapping autoimmune disorders.

Call for proposal

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EU contribution
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13,Kiinamyllynkatu 13
20520 TURKU / ABO

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