Abstract

We assessed the role of platelet activation markers (PMPs, Annexin V and CD62P on activated platelets), cytokines (IL-1 β, IL-4, IL-6, IFN- γ, GM-CSF, and TNF α), and soluble factors (sIL-2R, TM, sHLA-1, β2 -m sVCAM-l, sPECAM-1, sP-selectin and sE-selectin) in vascular damage related to SLE. There were differences in the levels of PMPs and platelet activation markers between the SLE patients and controls (PMPs: 493±82 vs. 328±36, p<0.05; plt-CD62P; 8.5%±1.2 % vs. 4.6%±0.7 %, p<0.05; plt-Annexin V: 11.3%±2.1 % vs. 4.9%±0.6 %, p<0.01). There were no differences in the levels of IFN- y between the groups. However, the levels of IL-11β IL-4, IL-6, GM-CSF, TNF α, and soluble factors were higher in the SLE patients than in the controls. The levels of IL-4, IL-6, p2-m, sIL-2R, sVCAM-1, sP-selectin, and sE-selectin in SLE patients with elevated sTM levels were higher than those in the SLE patients without elevated sTM levels. On the other hand, elevations of s[L-2R, sVCAM-l, and sP-selectin were not found in patients with Behcet disease or rheumatoid arthritis. The levels of platelet CD62P, platelet annexin V, and PMP were significantly elevated in high-sTM patients. These findings suggest the possibility that activated platelets and cytokines participate in the pathogenesis of SLE in patients with elevated sTM levels.

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