Timd4, also known as T cell immunoglobulin and mucin domain containing 4, is significantly involved in macrophage-related functions and various biological processes. It serves as an important receptor in efferocytosis, the clearance of apoptotic cells, which is crucial for tissue homeostasis and prevention of autoimmunity. Additionally, it may be associated with pathways like Wnt/β-catenin in certain cell types [1,3].

In mouse models, Timd4 deficiency leads to reduced CD301b+ macrophages and aggravated periodontitis bone loss, indicating its role in maintaining the osteoimmunology microenvironment in periodontitis [2]. In skin wound repair in mice, inhibition of Timd4 decreases efferocytosis and abrogates wound repair, highlighting its importance in the process of tissue repair [5]. In the context of cancer, Tim-4+ cavity-resident macrophages can impair anti-tumor CD8+ T cell immunity, and Tim-4 blockade can enhance anti-tumor efficacy in mouse models of immunotherapy [4].

In conclusion, Timd4 plays essential roles in macrophage-mediated processes such as efferocytosis, tissue repair, and immune regulation in various disease conditions. Studies using gene-knockout mouse models have provided valuable insights into its functions in periodontitis, skin wound repair, and cancer immunotherapy, suggesting that Timd4 could be a potential therapeutic target for these diseases.