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Xue and colleagues show that Runx3^−/− CD8⁺ T effector cells aberrantly upregulate genes characteristic of T_FH cell lineage and exhibit impaired induction of cytotoxic molecules.

The transcription factors TCF1 and LEF1 promote self-renewal and regulatory functions in B-1a cells.

Tumor-infiltrating CD8⁺ T cells acquire HOBIT expression and features of tissue-resident memory cells. This TGFβ-driven process is dispensable for tumor control by immune checkpoint blockade, but disrupting TGFβ signaling in HOBIT-expressing tumor-infiltrating lymphocytes enhances anti-tumor immunity.

Follicular helper T cells (T_FH cells) are specialized effector CD4⁺ T cells that help B cells develop germinal centers and memory. Crotty and colleagues show that the transcription factors LEF-1 and TCF-1 are required for early T_FH differentiation.

Xue and colleagues show that the transcription cofactor Tle3 cooperates with Runx3, Tcf1 and Tbet to limit a central memory and promote an effector memory cell signature in CD8⁺ T cells.

Xue and colleagues show that the transcription factors Tcf1 and Lef1 suppress CD4⁺ T lineage genes in CD8⁺ T cells through intrinsic histone deacetylase (HDAC) activity.

TCF-1 and LEF-1 are essential for early T cell development. Xue and colleagues show that in DP thymocytes, they control CD4⁺-versus-CD8⁺ T cell lineage 'decisions' and contribute to the establishment of CD8⁺ T cell identity.

Stemness is crucial for the maintenance of long-term T cell memory. Gattinoni and colleagues demonstrate that the transcription factor c-Myb is essential for the establishment of a stemness program in the CD8⁺ T cell memory compartment.

Ezh2 is an histone methyltransferase that catalyzes H3K27me3. Here the authors show that Ezh2 promotes T follicular helper (T_FH) differentiation and helper activity, by cooperating with Tcf1 to activate Bcl6 transcription and epigenetically repressing p19Arf, an antagonist of Bcl6 function and T_FH cell survival.

Xue and colleagues show that the transcription factor Tcf1 preprograms a transcriptional program that supports the bioenergetic and proliferative needs of CD8⁺ central memory T cells in case of a secondary challenge.

Xue and colleagues show that Tcf1 and Lef1 recruit the genome organizer CTCF to promote chromatin interactions and form highly connected, dynamic interaction hubs in CD8⁺ T cells undergoing homeostatic proliferation.

The cellular and molecular events that drive early innate lymphoid cell (ILC) development remain poorly understood. Bhandoola and colleagues used a reporter mouse to identify a new subset of early ILC progenitors (EILPs) that express high amounts of TCF-1.

Taniuchi and colleagues describe the generation and phenotype of a mouse model carrying a defective Bcl11b allele encoding a mutant protein corresponding to BCL11B-N441K previously associated with human disease. They further characterize the molecular interactions between the mutant BCL11B protein and other transcription factors involved in early thymocyte development.

The histone lysine methyltransferase MLL4 primes the locus encoding the transcription factor Foxp3 for transcriptional activation in thymus-derived and inducible regulatory T cells.

How CD8⁺ T cell identity is maintained after exit from the thymus is not fully established. Here the authors use multiomics approaches including Hi-C to show that Tcf1 and Lef1 prevent aberrant expression of lineage-inappropriate genes by organizing three-dimensional genomic architecture in CD8⁺ T cells.

The DNA-binding domains of transcription factors have been well characterized, but whether their intrinsically disordered regions control cell fate is unclear. Here, the authors show the functional and mechanistic importance of an intrinsically disordered region of TCF-1 in T cell development.

Bhandoola and colleagues show that the transcription factor TCF-1 restrains the dendritic cell lineage potential in innate lymphoid cell progenitors.

Acute myeloid leukaemia (AML) is maintained by self-renewing leukemic stem cells. Here the authors show that Heat Shock Transcription Factor 1 (HSF1) is specifically required for the maintenance of AML stem cells, while sparing steady-state and stressed haematopoiesis and that pharmacologically targeting HSF1 may have broad anti-leukemic effects.

Early humoral responses to malaria fail to induce durable protective antibodies. Butler and colleagues report that low-affinity, short-lived plasmablasts become nutrient sinks for glutamine and starve germinal center B and T cells, thereby reducing the generation of high-affinity B cells and long-lived plasma cells and memory B cells.

Harty and colleagues show that peripheral infections can establish and maintain functional antigen-specific tissue-resident memory CD8⁺ T cells in the central nervous system.

The expression of CD4, a critical co-receptor providing T cell help in adaptive immunity, is finely tuned during development. Here the authors show that two enhancer elements, E4p and the newly-defined E4m, coordinate the expression and heritable demethylation of Cd4 in thymocytes but are dispensable for its sustained expression in peripheral T cells.

Chronic infection with lymphocytic choriomeningitis virus promotes the establishment of a population of stem-like PD-1⁺ CD8⁺ T cells that reside in lymphoid tissues and preferentially expand when the PD-1 inhibitory pathway is blocked.

The transcription factor TCF1 is essential for early T cell development, and recent advances have uncovered context-dependent functions in mature T cells. This review summarizes key findings on TCF1 across the field of T cell immunity and explores their translational potential.