Tbx21, also known as T-Box Transcription Factor 21, is a crucial regulator of the type 1 immune response. It plays a vital role in coordinating multiple aspects of the immune response and is associated with various biological processes and diseases [1,2,3,4]. It is involved in pathways that impact cell proliferation, apoptosis, and immune cell function [1,2,3]. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its function.

In colorectal cancer (CRC), studies show that TBX21 expression is decreased in CRC tissues compared to normal tissue and is negatively correlated with CRC TNM stages. Ectopic expression of TBX21 inhibits cell proliferation, promotes apoptosis, and suppresses metastasis in CRC both in vitro and in vivo. RNA-seq and phospho-kinase array assays suggest that TBX21 acts via ARHGAP29/RSK/GSK3β and MYCT1/ZO-1 signaling pathways [1,5]. In microsatellite stable CRC, Fusobacterium nucleatum can induce Tbx21 promoter H3K27 acetylation and expression in CD8+ T cells, and TBX21 transcriptionally represses PD-1, alleviating CD8+ T cell exhaustion [2]. In CMS1 subtype CRC, high TBX21 expression and low methylation are associated with a survival advantage, and it is related to CTL infiltration [3].

In conclusion, Tbx21 is essential for the type 1 immune response and has significant impacts on cancer progression, especially in CRC. The use of KO or CKO mouse models in these studies has helped to reveal its role in regulating cell behavior and immune responses in the context of CRC and other related diseases.