Given that itself is a potent inducer of sTNFR production through its binding to the surface TNFR6, it is likely that increased sTNFR-II in ABD reflects overexpression. Several studies have reported that increased sTNFR-II serum levels correlate with disease activity in various inflammatory disorders in which a central pathogenetic role of has been proven7-9. In patients with systemic lupus erythematosus, in whom CRP is unable to differentiate disease activity, sTNFR-II correlates with clinical disease activity to a remarkable extent, even better than anti-DNA antibodies13'14. Along these lines, our results suggest that elevated levels of this molecule, predict indeed the presence of active disease probably reflecting the neutralization of increased TNF-a bioactivity.
Our findings on peripheral y8 T-cells are in accordance with previous reports, in which these T-cells have been also found in an increased number, not depending on the activity of ABD3'4. Since these T-cells overproduce TNF-a, one may expect that a positive correlation between y8 T-cells and sTNFR-II serum levels would exist in ABD. However, such correlation was not found, probably because we measured the total numbers of T-cells rather than their activated subset. In any case, whether the expansion of T-cells expressing TCRyS in ABD is a primary pathogenetic element or an epiphenomenon remains to be elucidated in further studies.
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