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Protein kinase signals activate interleukin 16 encoding transcripts in rheumatoid arthritis versus osteoarthritis synovial fibroblasts
  1. M K Schuler,
  2. S Sell,
  3. W K Aicher
  1. Centre for Orthopaedic Surgery, UKT University Hospital, Tübingen, Germany
  1. Correspondence to:
    Dr W K Aicher, Research Laboratory, University Medical Centre for Orthopaedic Surgery, Pulvermuehlstrasse 5, D 72070 Tübingen, Germany;

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Interleukin 16 (IL16) is a proinflammatory cytokine and a chemoattractant factor for CD4+ T cells. IL16 has been detected at higher concentrations in rheumatoid arthritis (RA) synovial fluid than in osteoarthritis(OA) specimens.1 IL16 is expressed in inflammatory infiltrates and in CD68 synovial lining cells of patients with RA as detected by in situ hybridisation.1–3

In this study we compared the modulation of IL16 steady state mRNA in synovial fibroblasts (SF) from six patients with RA and from three patients with OA. SF were prepared, expanded, and characterised as described previously.4 To examine the IL16 encoding transcript amounts, SF were incubated in complete medium for 24 or 48 hours in the presence of one of the following chemicals: 1 ng/ml phorbol-12-myristate-13-acetate (PMA), an activator of protein kinase C (PKC); 200 ng/ml ionomycin (Iono), a calcium ionophor; 10 μM of adenosine-3′,5′-cyclic monophosphate (cAMP), which stimulates protein kinase A (PKA); 10 nM okadaic acid (Oka), a phosphatase inhibitor; 10 μM MAS-7, which activates G-proteins; 100 μM H-7 dihydrochloride (H-7), …

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