CCL2 and keloid: To explain an aspect of such immunohistochemical differences, we formulated two hypotheses: firstly, scarring beneath the basal layer prevented basal cells from releasing MCP-1, as reported for keloid-derived fibroblasts [13], and secondly, accelerated release of MCP-1 exhausted significant amounts of MCP-1 from the cytoplasm of keratinocytes in the basal and parabasal layers.