Zfp683-flox Mouse

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.