To determine the cellular source of MCP-1 in innate immune responses, we utilized two mouse peritonitis models, induced by TG or zymosan A. The MCP-1 concentration in the exudates of myeloid cell-specific MCP-1-deficient mice was not decreased in either peritonitis model, indicating that non-myeloid cells are the primary source of MCP-1. This evidence concerns the gene CCL2 and peritonitis.