Slfn4, also known as Schlafen4, is associated with the differentiation and function of myeloid-derived suppressor cells (MDSCs) and is involved in multiple signaling pathways. It has been implicated in processes such as inflammation, oxidative stress, and metaplasia development. Genetic models, like gene-knockout mouse models, have been crucial in studying its function.

In ApoE -/-Slfn4 -/- double-deficient mice, the absence of Slfn4 significantly decreased inflammatory cell numbers within arterial plaques, limited atherosclerosis development, reduced pro-inflammatory cytokines, ROS generation, and apoptosis, and compromised the activation of MAPKs and apoptosis signaling pathways, indicating its role in modulating vascular inflammation and atherosclerosis [1]. In Gli1CreERT2 x Slfn4 fl/fl mice, in vivo disruption of Slfn4 after Helicobacter infection suppressed SLFN4 and NOS2, reversed T cell suppression, and mitigated spasmolytic polypeptide-expressing metaplasia (SPEM) development, suggesting that Slfn4 regulates the activity of the GTPase pathway in MDSCs during gastric metaplasia [2].

In conclusion, Slfn4 plays essential roles in regulating MDSC-related functions in processes such as vascular inflammation in atherosclerosis and gastric metaplasia. Gene-knockout mouse models have been instrumental in uncovering these functions, providing insights into its role in disease-related biological processes and potentially guiding future therapeutic strategies for associated diseases.