Eomes, short for Eomesodermin, is a transcription factor that plays crucial roles in the development and function of various immune cells. It is involved in the regulation of cell differentiation, function, and survival, and is associated with pathways related to immune responses against infections and tumors. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, have been valuable in studying its functions [1,2,3,4].

In immune cell development, Eomes expression identifies the early bone marrow precursor to classical NK cells, demonstrating that the NK and ILC1 lineages diverge early during development [1]. Eomes deletion in antigen-specific CD4+ T cells protects against central nervous system inflammation, as it is required for the long-term maintenance of CNS-infiltrating CD4+ T cells, and it promotes inflammation by enhancing CD4+ T cell mitochondrial functions [2]. Deleting T-BET and EOMES in unexpanded primary human NK cells compromises their in vivo antitumor response, as these transcription factors are needed for normal NK cell proliferation, persistence, and response to cytokine stimulation [3].

In conclusion, Eomes is essential for the development and function of multiple immune cell types. Through model-based research, especially KO/CKO mouse models, we have learned that Eomes is crucial in immune-related disease conditions such as central nervous system inflammation and in determining the efficacy of NK-cell-mediated antitumor responses. Understanding Eomes provides insights into immune-mediated disease mechanisms and potential immunotherapy strategies.