CD1 molecules present microbial and self glycolipid antigens to a defined T cell subset with features of natural killer cells. CD1 molecules are up-regulated by inflammatory stimuli such as GM-CSF, and we would expect to find increased CD1 expression in the synovium of patients with rheumatoid arthritis (RA) as compared to osteoarthritis (OA). This study was initiated to compare the density of CD1a+, CD1b+, and CD1c+ synovial cells in RA and OA patients.
Expression of CD1a+, CD1b+, and CD1c+ molecules in synovial tissue was assessed by semiquantitative immunohistochemistry. For comparison, serological, functional, and typical immunohistochemical markers of inflammation were detected.
Although patients with RA as compared to OA had highly significantly increased signs of inflammation, the density of CD1a+, CD1b+, and CD1c+ synovial cells was similar This was also true for the density of CD1+ cells in relation to that of activated CD163+ macrophages. There was a high correlation between the densities of CD1a,b,c positive cells, which suggests the existence of similar regulatory pathways. In a combined analysis of RA and OA patients, there existed a negative association between prior NSAID therapy and the density of CD1a+, CD1b+, and CD1c+ synoviocytes in relation to CD163+ macrophages. This is interesting because a similar immunosuppressive aspect of NSAID has never been shown before and this might represent a hitherto unrecognized immunosuppressive aspect of NSAID.
Considering the high synovial inflammation in patients with RA, the densities of CD1a+, CD1b+, and CD1c+ synovial cells were low compared to patients with OA. Further studies in RA patients are needed to clarify whether a defect in CD1 regulation may exist. Such a defect may lead to an insufficient immune response against microbial glycolipids, which would support smoldering or repeated inadequately responded infection.