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α-enolase expressed on the surfaces of monocytes and macrophages induces robust synovial inflammation in rheumatoid arthritis : alpha-enolase expressed on the surfaces of monocytes and macrophages induces robust synovial inflammation in rheumatoid arthritis

Cited 100 time in Web of Science Cited 104 time in Scopus
Authors

Bae, Seyeon; Kim, Hyemin; Lee, Naeun; Won, Cheolhee; Kim, Hang-Rae; Hwang, Young-il; Song, Yeong Wook; Kang, Jae Seung; Lee, Wang Jae

Issue Date
2012-07
Publisher
American Association of Immunologists
Citation
Journal of Immunology, Vol.189 No.1, pp.365-372
Abstract
alpha-Enolase (ENO1) is a multifunctional glycolytic enzyme expressed abundantly in the cytosol. It has been implicated in autoimmune and inflammatory diseases. Serum Abs against ENO1 were reported in rheumatoid arthritis (RA). Cell-surface expression of ENO1 has been found to be increased rapidly in response to inflammatory stimuli, but its expression and function has not been reported in RA. In this study, we show that cell-surface expression of ENO1 is increased on monocytes and macrophages isolated from RA patients but not on those from osteoarthritis patients, and Ab against ENO1 can stimulate these cells to produce higher amounts of proinflammatory mediators, such as TNF-alpha, IL-1 alpha/beta, IFN-gamma, and PGE2 via p38 MAPK and NF-kappa B pathway. The frequency of ENO1-positive cells in synovial fluid mononuclear cells was higher than PBMCs. ENO1-positive cells were also found in the inflamed synovium from RA patients and arthritic ankle tissues of mice with collagen-induced arthritis. Taken together, these findings suggest that Abs against ENO1 present in RA sera may stimulate monocytes and macrophages expressing cell-surface ENO1 and contribute to production of proinflammatory mediators during the effector phase of synovial inflammation. The Journal of Immunology, 2012, 189: 365-372.
ISSN
0022-1767
URI
https://hdl.handle.net/10371/202668
DOI
https://doi.org/10.4049/jimmunol.1102073
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Research Area Function, Immune modulation by metabolites, T-cell anergy, differentiation of memory CD8+ T cells, metabolism

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