TY - JOUR T1 - Clues to pathogenesis of spondyloarthropathy derived from synovial fluid mononuclear cell gene expression profiles. JF - The Journal of Rheumatology JO - J Rheumatol SP - 2159 LP - 2164 VL - 29 IS - 10 AU - Jieruo Gu AU - Markus Rihl AU - Elisabeth Märker-Hermann AU - Dominique Baeten AU - Jens G Kuipers AU - Yeong Wook Song AU - Walter P Maksymowych AU - Ruben Burgos-Vargas AU - Eric M Veys AU - Filip De Keyser AU - Helmuth Deister AU - Momiao Xiong AU - Feng Huang AU - Wen Chan Tsai AU - David Tak Yan Yu Y1 - 2002/10/01 UR - http://www.jrheum.org/content/29/10/2159.abstract N2 - OBJECTIVE: To use gene expression profiles of spondyloarthropathy (SpA) synovial fluid mononuclear cells (SFMC) to determine if there are transcripts that support the unfolded protein response (UPR) hypothesis, and to identify which cytokines/chemokines are being expressed and which cell fractions are involved. METHODS: Gene expression profiles were generated by microarray screening of SFMC of 5 patients with SpA, 5 patients with rheumatoid arthritis (RA), and peripheral blood mononuclear cells (PBMC) of 6 controls. Results were validated by reverse transcription polymerase chain reaction using samples from a larger panel of subjects. RESULTS: The repertoires of proinflammatory cytokines/chemokines expressed by SpA and RA SFMC were very similar: monocyte chemotractant protein 1 (MCP-1), interleukin 8 (IL-8), IL-1beta, endothelial-monocyte activating polypeptide II, interferon-gamma, and tumor necrosis factor-alpha. MCP-1 was highly expressed in SpA SFMC. There was enhanced expression of immunoglobulin heavy chain binding protein (BiP) in SpA, which is compatible with the UPR hypothesis. BiP was most highly expressed in the adherent fraction of SpA SFMC. CONCLUSION: Previous data postulating UPR in SpA are based on in vitro experiments with transfected cell lines. Our patient derived data suggest that it also occurs in vivo in the macrophages of SpA joints. ER -