4 results match your criteria: "Center for Rheumatic Diseases in Kangnam St. Mary's Hospital[Affiliation]"

NF-kappaB inhibition leads to increased synthesis and secretion of MIF in human CD4+ T cells.

Immunol Lett

March 2009

The Center for Rheumatic diseases in Kangnam St. Mary's Hospital, and Rheumatism Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea.

To examine the effects of nuclear factor kappa B (NF-kappaB) inhibition on the secretion of macrophage migration inhibitory factor (MIF) in human CD4(+) T cells. Isolated human CD4(+) T cells were cultured for 24h with pharmacological inhibitors of NF-kappaB including parthenolide, pyrrolidine dithiocarbamate, BAY 11-7082, gliotoxin, oridonin, andrographolide, and NF-kappaB shRNA. MIF concentration was measured by intracellular flow cytometry, enzyme-linked immunosorbent assay, and real-time polymerase chain reaction.

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Oral administration of type-II collagen suppresses IL-17-associated RANKL expression of CD4+ T cells in collagen-induced arthritis.

Immunol Lett

April 2008

The Center for Rheumatic Diseases in Kangnam St. Mary's Hospital and Rheumatism Research Center, College of Medicine, The Catholic University of Korea, Seoul, South Korea.

The receptor activator of nuclear factor kappaB ligand (RANKL) is an osteoclastogenic mediator, which is mainly expressed by stromal cells and osteoblast. However, T cells can also be an important provider for RANKL in special condition such as autoimmune arthritis. We examined the RANKL expression of hyporesponsive CD4+ T cells induced by oral feeding with type II collagen in collagen-induced arthritis (CIA) mice.

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Cyclosporine inhibition of vascular endothelial growth factor production in rheumatoid synovial fibroblasts.

Arthritis Rheum

May 2002

The Center for Rheumatic Diseases in Kangnam St. Mary's Hospital, and Research Institute of Immunobiology, Catholic Research Institutes of Medical Sciences, Catholic University of Korea, Seoul, Korea.

Objective: To determine the antiangiogenic effect of cyclosporin A (CSA) in rheumatoid arthritis (RA).

Methods: We investigated the effect of CSA on the production of vascular endothelial growth factor (VEGF) by rheumatoid synovial fibroblasts. Fibroblast-like synoviocytes (FLS) were prepared from the synovial tissues of RA patients, and cultured in the presence of CSA.

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We tested the impact of CD40 engagement on the production of vascular endothelial growth factor (VEGF) from rheumatoid synovial fibroblasts. Fibroblast-like synovial cells (FLS) were prepared from the synovial tissues of rheumatoid arthritis patients and cultured in the presence of CD40 ligand-transfected (CD40L+) L cells. VEGF levels were determined in the culture supernatants by ELISA.

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