Can we explain the varying pathologic processes of rheumatoid arthritis by CaMKII delta abnormality?

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We have examined the relationship between the pathogenesis of rheumatoid arthritis (RA) and CaMKII/PADIs/peptide citrullination/cellular abnormality of synovial cells and immune competent cells. Expression of PADIs in the rheumatoid synovial tissues remains to be clarified at present. According to our data, the expression of PADIs was weak whereas that of PADIs substrates were present in rheumatoid synovial cells. PADIs substrates in rheumatoid synovial cells could be citrullinated by interaction with neighboring immune competent cells, resulting in stimulation of anti-cyclic citrullinated peptide antibodies (anti-CCP antibodies) in patients with RA. Our present data also suggested that the function of regulatory T cells (Treg cells), a major immune competent cell population, is down-regulated in patients with RA that may associate with perpetuation of the disease's process. However, further investigation is necessary to identify whether these phenomena are primary events or secondary results. In addition, the investigations regarding to the association of Treg cells with CaMKII/PADIs are also be necessary. In clinical study, we have identified a close association of MRI-proven bone edema with anti-CCP antibodies. At present, a detection of peptide citrullination is very difficult. Therefore, we are also going to solve this problem by immune complexsome analysis.