Batf3, a transcription factor, is crucial for the development of mucosal conventional DCs type 1 (cDC1) [2]. It is also involved in various immune-related pathways, playing an important role in the cross-presentation of antigens, T cell-mediated immunity, and maintaining intestinal epithelial homeostasis. Genetic models, such as gene knockout (KO) mouse models, have been instrumental in studying Batf3's functions.

In Batf3 -/- mice, CD8α+ dendritic cell development was ablated, leading to defective cross-presentation and lack of virus-specific CD8+ T cell responses to West Nile virus. Also, rejection of highly immunogenic syngeneic tumors was impaired, suggesting a key role of CD8α+ dendritic cells and cross-presentation in responses to viruses and tumor rejection [1]. In another study, Batf3 -/- mice developed metabolic syndrome, had increased intestinal permeability, and altered microbiota, indicating that BATF3 protects against metabolic syndrome and preserves intestinal epithelial barrier by maintaining beneficial microbiota [2].

In conclusion, Batf3 is essential for the development of certain dendritic cell subsets, which are crucial for antiviral and anti-tumor immune responses. Its role in maintaining intestinal epithelial homeostasis and preventing metabolic syndrome is also significant. The Batf3 KO mouse models have been valuable in revealing these functions, providing insights into the mechanisms of immune-related diseases and metabolic disorders.

References:

1. Hildner, Kai, Edelson, Brian T, Purtha, Whitney E, Murphy, Theresa L, Murphy, Kenneth M. . Batf3 deficiency reveals a critical role for CD8alpha+ dendritic cells in cytotoxic T cell immunity. In Science (New York, N.Y.), 322, 1097-100. doi:10.1126/science.1164206. https://pubmed.ncbi.nlm.nih.gov/19008445/

2. Hamade, Hussein, Stamps, Jasmine T, Stamps, Dalton T, Targan, Stephan R, Michelsen, Kathrin S. 2022. BATF3 Protects Against Metabolic Syndrome and Maintains Intestinal Epithelial Homeostasis. In Frontiers in immunology, 13, 841065. doi:10.3389/fimmu.2022.841065. https://pubmed.ncbi.nlm.nih.gov/35812447/