Zfp683, also known as ZNF683 in humans, encodes the transcription factor Hobit. It is crucial for the tissue residency of certain lymphocytes. It is involved in the development of tissue-resident memory T (Trm) cells, natural killer T (NKT) cells, and liver-resident NK cells, and plays a role in the transcriptional program that enforces tissue retention of these cells [1].

In Zfp683 reporter mice, the correlation of Hobit expression with type 1 innate lymphoid cells (ILC1s) is tissue-and context-dependent. Zfp683 deletion led to a marked decrease in granzyme-and interferon-gamma (IFNγ)-producing ILC1s in the liver, slightly fewer ILC1s and more Eomes+ TCF1+ ILC1-like NK cells in salivary glands, and only reduced production of granzyme B by ILC1 in the intestinal mucosa. Ablation of Zfp683-dependent liver ILC1 led to increased viral load in the presence of intact adaptive and innate immune cells critical for mouse cytomegalovirus (MCMV) clearance [2,3].

In conclusion, Zfp683 is central to the tissue-resident lymphocyte transcriptional program, affecting ILC1 numbers and function in different tissues. Studies using Zfp683-related mouse models have revealed its importance in antiviral immunity, suggesting it may be a potential target for understanding and treating viral-related diseases.