MEC/CCL28 Protein, Human (His)

CCL28, also known as mucosal associated epithelial chemokine (MEC), CCK1, and SCYA28, is a chemokine. It is expressed in various mucosal sites, including salivary glands and mammary glands, trachea and colon, and small intestine. CCL28 has been classified as an important component chemokine in homeostasis lymphocyte transport and can bind to CCR3 and CCR10. Among them, CCL28 can chemotactic CCR10 expression of CD4 and CD8 T cell populations, as well as CCR3 expression of eosinophils migration. However, in the intestinal mucosa, few T cells express CCR10. In contrast, in the B-cell population, CCR10 can be selectively expressed by IgA plasma mother cells and IgA-secreting cells (i.e. plasma cells), which play a key role in homing plasma mother cells to extraintestinal effector sites^[1]. CCL28 is constitutively expressed in the colon, but its levels can be increased by pro-inflammatory cytokines and certain bacterial products that play a role in effector cell recruitment to sites of epithelial injury.CCL28 can act as a unifying immunostimulant on the mucosal surface and is involved in the migration of IgA-expressing cells to the breast, salivary glands, intestine, and other mucosal tissues. In addition, CCL28 exhibits broad-spectrum antimicrobial activity against Gram-negative and Gram-positive bacteria as well as fungi, such as Pseudomonas aeruginosa and Klebsiella pneumoniae. Further studies also showed that the positively charged amino acids at the C-terminal end of CCL28 significantly contributed to the antibacterial activity of the protein, and its characteristic hydrophobicity and amphiphilicity also contributed to its killing activity^[2].

CCL28 (human; 1 ng/mL, 48 h) has no effect on DSC growth, but promotes decidual stromal cells (DSCs) apoptosis, and blocking CCL28-CCR3/CCR1 signaling can inhibit CCL28-induced apoptosis^[3].
CCL28 (5, 2.5, 1.2 μg/mL, 2.5 h) can induce migration of IgA-secreting cells and IgA⁺ memory B cells from human H. pylori-infected tissues^[4].