RELT, short for Receptor Expressed in Lymphoid Tissues, is a member of the Tumor Necrosis Factor Superfamily. It is involved in cytokine signaling and pathways related to cell death or survival, and plays a role in various biological processes such as cancer development, immune system regulation, and development [1]. The RELT family also includes two paralogs, RELL1 and RELL2.

In mouse models, RELT -/- mice demonstrated that RELT deficiency selectively promotes the homeostatic proliferation of CD4+ T cells and enhances anti-tumor CD8+ T-cell responses, indicating that RELT negatively regulates the early phase of the T-cell response, probably by promoting T-cell apoptosis [2]. In another study, mutations in RELT in humans cause autosomal recessive amelogenesis imperfecta, and Relt -/- mice generated by CRISPR/Cas9 showed incisor and molar enamel malformations, suggesting RELT's importance in tooth development [3].

In conclusion, RELT is crucial for immune system regulation and tooth development. The RELT knockout mouse models have provided insights into its role in these biological processes, highlighting its significance in understanding immune-related diseases and amelogenesis imperfecta.

References:

1. Cusick, John K, Alcaide, Jessa, Shi, Yihui. 2023. The RELT Family of Proteins: An Increasing Awareness of Their Importance for Cancer, the Immune System, and Development. In Biomedicines, 11, . doi:10.3390/biomedicines11102695. https://pubmed.ncbi.nlm.nih.gov/37893069/

2. Choi, Beom K, Kim, Seon-Hee, Kim, Young H, Lee, Ho, Kwon, Byoung S. 2018. RELT negatively regulates the early phase of the T-cell response in mice. In European journal of immunology, 48, 1739-1749. doi:10.1002/eji.201847633. https://pubmed.ncbi.nlm.nih.gov/30138536/

3. Kim, Jung-Wook, Zhang, Hong, Seymen, Figen, Simmer, James P, Hu, Jan C-C. 2018. Mutations in RELT cause autosomal recessive amelogenesis imperfecta. In Clinical genetics, 95, 375-383. doi:10.1111/cge.13487. https://pubmed.ncbi.nlm.nih.gov/30506946/