MDC/CCL22 Protein, Human

CCL22, also known as macrophage-derived chemokine (MDC), a CC chemokine located on chromosome 16 in the human genome, is a protein encoded by the CCL22 gene that shares 37% identity with CCL17 at the amino acid level. CCL22 is secreted by dendritic cells and macrophages and can be upregulated by a variety of stimulatory factors, such as lipopolysaccharides, cytokines. Among them, the Th2 cytokines IL-4 and IL-13 induce CCL22 production in myeloid cells and can be inhibited by the Th1 cytokine IFN-γ. In addition to acting as a potent chemotactic agent for CCR4-expressing Th2 lymphocytes, monocytes, monocyte-derived dendritic cells, and natural killer cells, CCL22 can also affect its target cells by interacting with the chemokine receptor CCR4. CCL22 is a potent inducer of CCR4 internalization, and CCL22 binding to CCR4 reduces the subsequent functional response of CCR4. The interaction of CCL22 with CCR4 is involved in a variety of pathologies, ranging from allergic reactions and autoimmunity to tumor growth. In contrast, small molecule compounds and antibodies capable of blocking CCL17 and CCL22-mediated recruitment of Th2 and Treg cells have been shown to have positive effects in various disease models of asthma, atopic disease and tumor growth. In addition, an important role of CCL22 and its receptors in TH2 lymphocyte recruitment has been shown in models of allergic airway inflammation. It can also be involved in thymopoiesis by regulating the migration of mature thymocytes through this organ^[1][2].

CCL22/MDC (100 ng/mL, 24 h) treatment alone dose not result in increased production of chemokine IL-8, and treatment of hBEC with TNF-α increased IL-8 secretion. In addition, treatment of hBEC with both TNF-α and MDC results in increased IL-8 production than treatment with TNF-α alone in human bronchial epithelial cells (hBEC)^[3].