Cd5l, also known as CD5 molecule-like, is a secreted glycoprotein. It plays crucial roles in inflammatory responses, being involved in processes such as infection, atherosclerosis, and cancer. In macrophages, it controls key mechanisms related to cytokine profiles and macrophage polarization. It is also a canonical component of circulatory IgM [1,4].

Cd5l-deficient mice exhibit impaired neutrophil recruitment and compromised bacterial control, making them more susceptible to cecal ligation and puncture-induced sepsis, highlighting its importance in sepsis-related immune responses [3]. In the context of cancer, high tumor-associated macrophage (TAM) expression of CD5L in papillary lung adenocarcinoma is associated with poor patient outcome. Blocking CD5L with a monoclonal antibody can inhibit the immunosuppressive phenotype of macrophages in vitro and tumor progression in vivo, altering the tumor microenvironment [2]. In renal fibrosis, the expression of CD5L is upregulated in end-stage renal disease patients and in a mouse model of unilateral ureteral occlusion. Recombinant CD5L injection in mice promotes renal injury, fibrosis, and phenotypic transfer of monocytes, while the CD5L antibody can reduce renal fibrosis [5].

In conclusion, Cd5l is a multifunctional protein involved in inflammation, immunity, and disease processes. Studies using gene-knockout mouse models have revealed its significance in sepsis, cancer, and renal fibrosis, providing insights into its potential as a therapeutic target in these disease areas.