Ccl28, a β-or CC chemokine, is involved in host immunity at various epithelial and mucosal linings. It plays a role in guiding the chemotactic activity of immune cells through interactions with its receptors CCR10 and CCR3. Ccl28 also has antimicrobial activity against bacteria and fungi, and is associated with lymphocyte trafficking and immunomodulation [2].

In gene knockout models, Alkbh5-knockout mice, where Ccl28 is a target of ALKBH5, show milder I/R-induced renal injury. The deficiency of Alkbh5 increases Ccl28 mRNA stability, leading to up-regulated Treg recruitment and inhibited inflammatory cells, suggesting a role of Ccl28 in the Treg/inflammatory cell axis regulation in acute kidney injury [1]. Ccl28-/-mice show different susceptibilities to Salmonella gut and Acinetobacter lung infections, indicating its critical role in immune response to mucosal pathogens by modulating neutrophil accumulation and activation [3]. In pancreatic cancer, CCL28 knockdown impairs the proliferation of mouse pancreatic cancer cells and remodels the tumor microenvironment by suppressing the infiltration of certain immune cells, suggesting its role in cancer progression [4].

In conclusion, Ccl28 is crucial for immune responses at mucosal surfaces, including antimicrobial defense, neutrophil modulation, and lymphocyte trafficking. Gene knockout models have revealed its significance in diseases such as acute kidney injury and pancreatic cancer, highlighting its potential as a therapeutic target in these disease areas.