Klrd1, also known as Killer Cell Lectin Like Receptor D1 or CD94, plays a crucial role in the immune system, especially in natural killer (NK) cells. It is involved in NK cell-mediated cytotoxicity and T cell receptor pathways, and is associated with antitumor immunity [3]. Genetic models, such as the mouse models with Klrd1-related mutations, are valuable for studying its function.

In influenza susceptibility studies, the expression of Klrd1 in NK cells was found to be inversely correlated with symptom severity. Lower Klrd1 expression in symptomatic shedders at baseline was observed in both discovery and validation cohorts, suggesting that an early response by Klrd1-expressing NK cells may control influenza infection [1].

In acute myocardial infarction and stable coronary artery disease, Klrd1 was identified as a potential biomarker for plaques progression, with high-expression at 1 day after myocardial infarction compared to the SHAM group [2].

In the context of pregnancy, the CD94/NKG2A inhibitory receptor, encoded in part by Klrd1, is important for optimizing pregnancy outcomes. Genetic ablation of NKG2A in dams led to suboptimal maternal vascular responses, perturbed placental gene expression, and reduced fetal weight, resembling features of pre-eclampsia [4].

In conclusion, Klrd1 is essential in immune-related functions, influencing disease states such as influenza susceptibility, plaques progression in cardiovascular diseases, and pregnancy outcomes. Mouse models with genetic modifications of Klrd1 have been instrumental in revealing these roles, contributing to our understanding of the underlying mechanisms in these specific disease areas.