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*
Department of Medicine, Division of Rheumatology, 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; and
Department of Microbiology, Kangwon National University, Chunchon, Korea
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.
Stimulation of FLS by CD40L+ L cells increased the
production of VEGF by 4.1-fold over the constitutive levels of
unstimulated FLS. The CD40L on activated T cells from rheumatoid
synovial fluid also up-regulated VEGF production from FLS. Neither
indomethacin nor Abs to IL-1ß, TNF-
, and TGF-ß did affect
CD40L-induced VEGF production. Stimulation of FLS with TNF-,
IL-1ß, and TGF-ß increased VEGF production by 1.6-, 2.0-, and
5.2-fold, respectively, and displayed an additive effect on the
production of VEGF by CD40L. VEGF mRNA expression was also up-regulated
by the stimulation of FLS with membranes from the CD40L+ L
cells. Dexamethasone completely abrogated CD40L-induced VEGF
production. In addition, pyrrolidine dithiocarbamate partially
down-regulated CD40L-induced VEGF production, showing that the NF-
B
pathway was partly involved in the signaling of CD40L leading to VEGF
production. Collectively, these results suggest that the interaction
between CD40 on synovial fibroblasts and CD40L expressed on activated T
lymphocytes may be directly involved in the neovascularization in
rheumatoid synovitis by enhancing the production of
VEGF.
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