RT Journal Article
SR Electronic
T1 Clues to pathogenesis of spondyloarthropathy derived from synovial fluid mononuclear cell gene expression profiles.
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 2159
OP 2164
VO 29
IS 10
A1 Jieruo Gu
A1 Markus Rihl
A1 Elisabeth Märker-Hermann
A1 Dominique Baeten
A1 Jens G Kuipers
A1 Yeong Wook Song
A1 Walter P Maksymowych
A1 Ruben Burgos-Vargas
A1 Eric M Veys
A1 Filip De Keyser
A1 Helmuth Deister
A1 Momiao Xiong
A1 Feng Huang
A1 Wen Chan Tsai
A1 David Tak Yan Yu
YR 2002
UL http://www.jrheum.org/content/29/10/2159.abstract
AB 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.