Btnl2, or butyrophilin-like protein 2, is a molecule with sequence homology to the B7 family members. It functions to inhibit T cell activation, regulating the immune response [3]. It has been associated with multiple biological pathways and is of significance in various disease conditions. Genetic models, especially KO mouse models, have been instrumental in studying its functions.

In KO mouse models, Btnl2 has been shown to be required for colorectal IL-22 production. Btnl2 knockout mice display decreased colonic tumorigenesis and more severe colitis phenotypes due to defective IL-22 production. Mechanistically, it acts on group 3 innate lymphoid cells (ILC3s), CD4+ T cells, and γδ T cells to promote IL-22 production [1]. Antibody-mediated blockade of Btnl2 in murine tumour models attenuates tumour progression, as Btnl2 interacts with local γδ T cell populations to promote IL-17A production in the tumour microenvironment, facilitating tumour immune escape [2].

In conclusion, Btnl2 plays a crucial role in regulating immune-related biological processes. Studies using Btnl2 KO mouse models have revealed its significance in colorectal tumorigenesis, colitis, and tumour immune escape. These findings provide potential therapeutic targets for diseases such as colorectal cancer, inflammatory bowel diseases, and other cancer immunotherapy-related conditions.