AbstractTo examine whether abnormalities in essential fatty acid (EFA) metabolism are associated with the impaired natural killer (NK) cell functions in primary Sjogren's syndrome, we measured the levels of phospholipid fatty acids in blood mononuclear cells with (MD) and without monocyte depletion (MC), and NK cell activity before and after indomethacin-boosting. We found MD levels of 20:3n6 (dihommo- gamma-linolenic acid), and basal and indomethacin-enhanced NK cell activity significantly reduced, in 10 primary Sjogren's syndrome patients as compared with 10 healthy controls. In the controls the relative (%) increase in indomethacin-enhanced NK cell activity correlated with the level of MD 18:2n6 (linoleic acid) (r = 0.97, p less than 0.001). In the patients the relative (%) indomethacin-enhanced NK cell activity correlated with the 20:4n6 (arachidonic acid)/20:3n6 ratio in the MC (r = 0.90, p less than 0.001). This ratio has been assumed to be an important determinant for the production of prostaglandin 1 and 2. The present data suggest that in healthy persons, as opposed to primary Sjogren's syndrome patients, the level of MD 18:2n6 is a determinant for the sensitivity of NK cells to monocyte- derived prostaglandins. Furthermore, in patients with primary Sjogren's syndrome the MC levels of 20:3n6 and 20:4n6 may be regulating factors for the production of NK cell suppressing prostaglandins.
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