Cd200, a cell surface glycoprotein, is an immunoregulatory ligand. It interacts with its receptor CD200R, playing a significant role in regulating immune responses. The CD200-CD200R pathway is involved in multiple immunoregulatory processes, such as controlling inflammation, and has implications in various biological contexts including transplant rejection, and diseases like infection, autoimmune diseases, and allergy [3].

In asthma, dysregulation of the CD200 pathway is linked to the disease, and pharmacological modulation of CD200 receptors can improve clinical and inflammatory outcomes in pre-clinical asthma models, suggesting it could be a target to alleviate asthma exacerbation [1]. In pancreatic ductal adenocarcinoma (PDAC), CD200 expression in the tumor microenvironment promotes immunosuppression by enhancing the expansion and activity of myeloid-derived suppressor cells (MDSC). In vivo antibody blocking of CD200 in mouse models limits tumor progression and enhances the efficacy of PD-1 checkpoint antibodies [2]. In early diabetes-related retinopathy, dysregulated CD200-CD200R signaling between amacrine cells and microglia contributes to microglia-mediated neurodegeneration, and targeting CD200R can prevent visual dysfunction and retinal inflammation in diabetic mice [4].

In conclusion, Cd200 is crucial in immunoregulation. Gene-knockout (KO) or conditional-knockout (CKO) mouse models have been instrumental in revealing its role in diseases such as asthma, PDAC, and diabetic retinopathy. These models help us understand how Cd200 and its receptor interaction can influence disease-related biological processes, providing potential targets for therapeutic interventions.