Klrd1, also known as Killer Cell Lectin Like Receptor D1, encodes CD94. It is expressed on natural killer (NK) cells and plays a crucial role in the immune system, being involved in pathways such as NK cell-mediated cytotoxicity and T cell receptor pathways. Genetic models like the mouse models are valuable for studying Klrd1 [4].

In influenza susceptibility studies, Klrd1-expressing NK cells were identified as a potential biomarker. Lower Klrd1 expression in symptomatic shedders at baseline was associated with increased symptom severity, suggesting that an early response by Klrd1-expressing NK cells may control influenza infection [1]. In the context of myocardial infarction and coronary artery disease, Klrd1 was screened out as a potential biomarker for plaques progression. In mouse MI models, Klrd1 was highly expressed 1 day after MI compared to the SHAM group [2]. In a study on spontaneous abortion, Klrd1 (CD94) was part of the complex regulatory network related to decidual NK cell residence. Although not directly from a Klrd1 KO/CKO model, it was in the context of autophagy-mediated NK cell-related mechanisms [3]. In head and neck squamous cell carcinoma (HNSC), Klrd1 is an independent prognostic factor, with high expression in NK and exhausted CD8+ T cells, and is involved in immune-related signaling pathways [4]. In pulmonary ischaemia-reperfusion injury, CD94+ NK cells potentiated the injury, and anti-CD94 monoclonal antibodies showed potential therapeutic benefit in mouse and human models [5].

In summary, Klrd1 is essential in the immune system, with its expression levels correlating with disease states in various conditions such as influenza susceptibility, myocardial infarction, and HNSC. Mouse models have been valuable in understanding its role in diseases like myocardial infarction and pulmonary ischaemia-reperfusion injury, highlighting its significance in disease pathogenesis and potential as a therapeutic target.

References:

1. Bongen, Erika, Vallania, Francesco, Utz, Paul J, Khatri, Purvesh. 2018. KLRD1-expressing natural killer cells predict influenza susceptibility. In Genome medicine, 10, 45. doi:10.1186/s13073-018-0554-1. https://pubmed.ncbi.nlm.nih.gov/29898768/

2. Zhang, Qiang, Zheng, Yue, Ning, Meng, Li, Tong. 2021. KLRD1, FOSL2 and LILRB3 as potential biomarkers for plaques progression in acute myocardial infarction and stable coronary artery disease. In BMC cardiovascular disorders, 21, 344. doi:10.1186/s12872-021-01997-5. https://pubmed.ncbi.nlm.nih.gov/34271875/

3. Lu, Han, Yang, Hui-Li, Zhou, Wen-Jie, Li, Da-Jin, Li, Ming-Qing. 2020. Rapamycin prevents spontaneous abortion by triggering decidual stromal cell autophagy-mediated NK cell residence. In Autophagy, 17, 2511-2527. doi:10.1080/15548627.2020.1833515. https://pubmed.ncbi.nlm.nih.gov/33030400/

4. Dong, Chengyuan, Lin, Ziyou, Hu, Yunzhao, Lu, Qun. 2025. KLRD1 (CD94): A Prognostic Biomarker and Therapeutic Candidate in Head and Neck Squamous Cell Carcinoma. In Journal of Cancer, 16, 982-995. doi:10.7150/jca.104762. https://pubmed.ncbi.nlm.nih.gov/39781341/

5. Tsao, Tasha, Qiu, Longhui, Bharti, Reena, Greenland, John R, Calabrese, Daniel R. 2024. CD94+ natural killer cells potentiate pulmonary ischaemia-reperfusion injury. In The European respiratory journal, 64, . doi:10.1183/13993003.02171-2023. https://pubmed.ncbi.nlm.nih.gov/39190789/