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Departments of
*
Oncology and
Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada; and
Berlex Laboratories, Richmond, CA 94806
IL-10, a cytokine with important anti-inflammatory properties,
is generated within the CNS during neuroinflammation. The mechanism for
its production is poorly understood. Since infiltrating lymphocytes
come into close proximity with the macrophage-like cells of the CNS,
the microglia, we have used an in vitro human microglia-T cell
coculture system to address the mechanisms of IL-10 production. We
demonstrate that microglia or activated T cells alone secrete
negligible amounts of IL-10, but that their coculture results in
significant IL-10 production, which was effected by both cell types.
IL-10 generation was cell contact dependent, and treatment with
anti-CD40, CTLA-4-Fc, or anti-CD23 decreased the IL-10 content
in microglia-T cell cocultures. The combination of anti-CD40 and
CTLA-4-Fc reduced IL-10 levels to the negligible amounts seen with T
cells or microglia in isolation. By also measuring TNF-
levels,
specificity of cytokine regulation was observed; while anti-CD40
and CTLA-4-Fc reduced IL-10 and TNF- levels, anti-CD23 did not
affect TNF- while attenuating IL-10 generation. Anti-very late Ag-4,
which decreased TNF- levels, did not affect IL-10. These results
implicate the CD40, B7, and CD23 pathways in IL-10 production following
microglia-T cell encounter and have relevance to the regulation of an
anti-inflammatory response within the CNS.
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