Mast cells, which derive from a bone marrow progenitor and mature in tissues, are important for allergic reactions, but also in inflammation, autoimmunity, and T-cell-mediated immune responses. The addition of certain cytokines to human umbilical cord blood-derived cultured mast cells have been shown to augment IgE-induced production of distinct cytokines, without histamine secretion. CCL2/MCP-1 is a beta chemokine capable of attracting and activating lymphocytes, macrophages, memory T cells and basophilic cells, but not neutrophils. CCL2/MCP-1 regulates the recruitment of inflammatory cells into tissue during inflammation and allergy. IL-33 belongs to the IL-1 family and binds to the ST2 receptor which has high homology to IL-1 receptor and has biological activities. IL-33, causes allergic inflammation and exerts significant biological effects both in vivo and in vitro. IL-33 induces expression of several cytokines and chemokines, resulting in severe inflammatory and allergic diseases. However, our knowledge regarding the effects of these cytokines on human mast cell functions is limited. Here, using human umbilical cord blood mast cells (HUCBMCs) as a valid model, we found that IL-33 induces CCL2/MCP-1 release in HUCBMCs. The release was higher at 24 h incubation compared with 12 h. This study documents the ability of IL-33 to directly stimulate Human umbilical cord blood mast cells (UCBMCs) to produce CCL2/MCP-1. We show that IL-33 is a strong activator of human mast cells capable of inducing CCL2/MCP-1 released at translational level. The present data describe an additional biological activity of IL-33, suggesting that this cytokine may have an important effect on the recruitment of inflammatory cells in allergic diseases.