NLRC5, also known as NOD4 or NOD27, is the largest member of the NLR (nucleotide-binding domain leucine-rich repeat containing) family. It acts as a transcriptional activator of MHC class I genes, participates in regulating cancer immune escape, and is involved in innate and adaptive immune responses. It also plays a role in multiple signaling pathways such as NF-κB, type I interferon, and inflammasome signaling pathways [2,3,4].

NLRC5-deficient mice were protected in hemolytic and inflammatory models, suggesting that NLRC5 could be a potential therapeutic target in these conditions. In endometriosis, inhibition of NLRC5 expression promotes the development of ectopic lesions, upregulates pro-inflammatory factors, and downregulates anti-inflammatory factors [1,5].

In conclusion, NLRC5 is crucial in immune responses, cancer immune surveillance, and inflammatory regulation. Gene knockout (KO) mouse models have revealed its role in hemolytic, inflammatory diseases, and endometriosis, providing insights into potential therapeutic strategies for these conditions.