Havcr1, also known as T-cell immunoglobulin and mucin domain 1 (TIM-1) and hepatitis A virus cellular receptor 1, is a type-1 integral membrane glycoprotein. It has a key role in immunity, renal regeneration, and acts as a receptor for hepatitis A virus [4,6]. It may also be involved in cancer-associated signaling pathways [5]. Genetic models, such as gene knockout in mice, are valuable for studying its functions.

In B cells, selective deletion of Havcr1 substantially inhibited tumour growth and enhanced effector T cell responses in a B16F10 melanoma mouse model. Loss of TIM-1 enhanced the type 1 interferon response in B cells, leading to increased B cell activation, antigen presentation, and co-stimulation, ultimately promoting the expansion of tumour-specific effector T cells [1]. In a high-fat-fed streptozotocin mouse model of diabetic kidney disease (DKD), genetic ablation of the KIM-1 (a product of Havcr1) mucin domain ameliorated tubule injury associated with DKD [2]. Placenta-specific Havcr1 deletion in mice significantly impaired Zika virus (ZIKV) transplacental transmission and associated adverse pregnancy outcomes, highlighting its role in ZIKV vertical transmission [3].

In conclusion, Havcr1 is crucial in multiple biological processes and disease conditions. Gene knockout mouse models have revealed its role in anti-tumour immunity, DKD, and ZIKV vertical transmission. These findings contribute to understanding the pathogenesis of related diseases and may provide potential therapeutic targets.