Btnl2, or butyrophilin-like protein 2, is a member of the immunoglobulin superfamily. It has been shown to regulate T cell activation [5]. BTNL2 is involved in pathways related to immune responses and homeostasis, playing an important role in various biological processes, especially those related to immune-mediated diseases [3,5].

In mouse models, BTNL2 knockout mice show decreased colonic tumorigenesis and more severe colitis phenotypes due to defective production of IL-22, as BTNL2 acts on group 3 innate lymphoid cells (ILC3s), CD4+ T cells, and γδ T cells to promote IL-22 production [1]. Also, 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 [2]. Moreover, in non-obese diabetic (NOD) mice, administration of rBTNL2-Ig ameliorates type 1 diabetes, associated with inhibiting autoreactive T cell proliferation, activation, and inflammatory cytokine production, while increasing regulatory T cell generation [4].

In conclusion, Btnl2 is crucial in regulating immune-related processes. Mouse knockout models have revealed its role in diseases such as colitis-associated tumorigenesis, tumour immune escape, and type 1 diabetes, providing potential therapeutic targets for these diseases.