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*
Departments of Pathology and
Internal Medicine, Division of Pulmonary and Critical Care, University of Michigan Medical School, Ann Arbor, MI 48109; and
Department of Pathology, Veteran Affairs Medical Center, Ann Arbor, MI 48105
This study addressed the role of endogenous monocyte
chemoattractant protein-1 (MCP-1) in Ag-stimulated lymphokine synthesis
and proliferation by CD4+ T cells during their
coculture with purified lung fibroblasts or splenic macrophages.
Initial experiments showed that fibroblasts exposed to IL-4, TNF 
,
or IL-4 and TNF- (all at 10 ng/ml) for 24 h released five- to
eightfold more MCP-1 than similarly treated splenic macrophages. In
72-h coculture experiments, the synthesis of IL-4 by OVA-activated
CD4+ T cells added to lung fibroblasts or splenic
macrophages was significantly inhibited when endogenous MCP-1 was
neutralized using polyclonal anti-MCP-1 antiserum. In these same
cocultures, IFN-
levels were significantly enhanced. Similarly,
IFN- levels were significantly enhanced in 72-h cocultures of a
purified peptide derivative-activated CD4+ Th1 clone and
lung fibroblasts or splenic macrophages following immunoneutralization
of MCP-1. In separate experiments, the selective inhibition of MCP-1
synthesis by lung fibroblasts and splenic macrophages using an MCP-1
antisense oligonucleotide significantly enhanced the proliferation of
CD4+ T cells during a 96-h coculture. Taken together, these
data suggest that MCP-1 exerts an immunomodulatory effect on
CD4+ T cell-derived IL-4 and IFN- release and
CD4+ T cell proliferation during cell-to-cell interactions.
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