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Rheumatology 2005 44(Supplement 3):iii21; doi:10.1093/rheumatology/keh772
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Supplement Article

PP19. NO MODIFICATION OF SIL-6R AND GP130 SERUM LEVELS IN ACTIVE AND TREATED PMR PATIENTS

R. Meliconi, P. Dolzani, T. Silvestri, L. Pulsatelli, C. Salvarani, P. Macchioni, L. Boiardi and A. Facchini

Modulo di Reumatologia Istituti Ortopedici Rizzoli, Bologna, Italy

Background: PMR patients have high systemic levels of IL-6 which correlate with prognosis. IL-6 mediates its activity through two membrane proteins: IL-6R and gp 130 (signal transducing element). Soluble complexes of IL-6R and IL-6, are able to associate to membrane-bound gp130 and thus they mediate intracellular signalling in IL-6R negative cells. Biological activity of sIL-6R/IL-6 complexes can be blocked by soluble gp130. We investigated the modulation of systemic levels of sIL-6R and gp130 in patients both in active disease and during corticosteroid treatment and the ability of peripheral blood mononuclear cells (PBMC) to contribute to circulating levels of these molecules.

Methods: We analyzed sIL-6R and gp 130 serum levels in 44 PMR patients at disease onset and after 1, 3, 6, 12, 24 months of follow-up and in 46 age-matched normal controls (NC). Furthermore we analyzed the ability of PBMC isolated from 13 untreated PMR patients and 13 healthy subjects to release sIL-6R and gp130 in basal condition and upon stimulation with lipopolysaccharide (LPS) and anti-CD3. Serum and supernatant levels were determined by ELISA.

Results: No difference in sIL-6R and gp 130 serum levels were noted between PMR and NC cases, either at disease onset or during follow-up. On the contrary, sIL-6R and gp130 production by PBMC obtained from untreated PMR patients was significantly higher compared to NC either in basal condition or after stimulation with LPS and anti-CD3.

Conclusions: At variance with other inflammatory diseases, we showed neither increase of sIL-6R serum levels nor decrease gp130 levels. Increased production by PMR PBMC does not modify normal serum levels.


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