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on Macrophage Inflammatory Protein-3 Production in Rheumatoid Arthritis: Regulation by Soluble Receptors and Th2 Cytokines1
Departments of Immunology and Rheumatology and Institut National de la Santé et de la Recherche Médicale, Unité 403, Hôpital Edouard Herriot, Lyon, France
Macrophage inflammatory protein (MIP)-3
is a chemokine involved
in the migration of T cells and immature dendritic cells. To study the
contribution of proinflammatory cytokines and chemokines to the
recruitment of these cells in rheumatoid arthritis (RA) synovium, we
looked at the effects of the monocyte-derived cytokines IL-1
and
TNF- and the T cell-derived cytokine IL-17 on MIP-3 production by
RA synoviocytes. Addition of IL-1, IL-17, and TNF- induced
MIP-3 production in a dose-dependent manner. At optimal
concentrations, IL-1 (100 pg/ml) was much more potent than IL-17
(100 ng/ml) and TNF- (100 ng/ml). When combined at lower
concentrations, a synergistic effect was observed. Conversely, the
anti-inflammatory cytokines IL-4 and IL-13 inhibited MIP-3
production by activated synoviocytes, but IL-10 had no effect. Synovium
explants produced higher levels of MIP-3 in RA than osteoarthritis
synovium. MIP-3-producing cells were located in the lining layer and
perivascular infiltrates in close association with CD1a immature
dendritic cells. Addition of exogenous IL-17 or IL-1 to synovium
explants increased MIP-3 production. Conversely, specific soluble
receptors for IL-1, IL-17, and TNF- inhibited MIP-3
production to various degrees, but 95% inhibition was obtained only
when the three receptors were combined. Similar optimal inhibition was
also obtained with IL-4, but IL-13 and IL-10 were less active. These
findings indicate that interactions between monocyte and Th1
cell-derived cytokines contribute to the recruitment of T cells and
dendritic cells by enhancing the production of MIP-3 by
synoviocytes. The inhibitory effect observed with cytokine-specific
inhibitors and Th2 cytokines may have therapeutic
applications.
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