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Background Rheumatoid arthritis (RA) is characterized by an inflammatory and destructive infiltration of various immune cells into the synovium of the joint. The first cells to arrive at the site of inflammation and the main cell type in synovial fluid are neutrophil granulocytes that locally release cytotoxic agents, antimicrobial peptides, proteases, and other inflammatory mediators, thus fuelling inflammation and damaging tissue. The aim of this project is to elucidate if locally released anti-microbial peptides contribute to the pathogenic events of arthritis.

The anti-microbial peptide rCRAMP is strongly upregulated during experimental arthritis in the rat