BATF3
- Known as:
- BATF3
- Catalog number:
- 002428A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BATF3
Related genes to: BATF3
- Gene:
- BATF3 NIH gene
- Name:
- basic leucine zipper ATF-like transcription factor 3
- Previous symbol:
- -
- Synonyms:
- JUNDM1, SNFT, JDP1
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-17
- Date modifiied:
- 2016-06-28
Related products to: BATF3
Related articles to: BATF3
- While CAR-T cell therapy has transformed outcomes in B-cell malignancies, most genomic insights originate from clinical trials. There is a paucity of data describing molecular changes during CAR-T manufacturing in real-world practice, particularly for non-US CAR constructs. - Source: PubMed
Publication date: 2026/09/03
Das NupurMehta PrashantGupta KusumKatharia RahulPabbi SwatiMishra PravasMorya Soni - Oncolytic virus M1 encoding a mutant IL-18 decoy (OVM18) represents a novel virotherapy that integrates selective oncolysis with localized activation of the IL-18 pathway. However, the heterogeneity of therapeutic responses suggests that host immune determinants influence its efficacy. - Source: PubMed
Publication date: 2026/09/07
Lin XueyingZhang JifuFan ZhenYang JingyuYi ShimingWang HanruiZou HuizhenHu LinyiZhu WenboLin YuanHu JunCai JingYan GuangmeiLiang Jiankai - Stimulator of interferon genes (STING) agonists have shown limited antitumor efficacy, in part because STING activation is not preferentially focused on dendritic cells (DCs), which specialize in cross-priming. We present a DC-centric strategy that synergistically licenses DCs by coordinating CD47-SIRPα checkpoint relief and STING activation via dual ultra-pH-sensitive gating. Mild tumor acidity first unmasks the αCD47 cue to prime antigen acquisition. Following DC-biased uptake, a second acidic gate releases cGAMP to engage STING in antigen-bearing DCs. Functionally, efficacy requires Batf3-dependent cDC1s and CD8 T cells, yet is preserved after macrophage depletion. In murine models, this strategy suppresses tumor growth and metastasis with good tolerability, and it retains activity in a humanized cell-line-derived xenograft model established in NSG-SGM3 hosts, supporting activity in a partially reconstituted human immune setting. Together, this work presents a mechanism-guided combination strategy to optimize STING agonist therapy. - Source: PubMed
Publication date: 2026/09/07
Xiang ShutingMa ShanshanXu TuzhiYu WenwenWang JiefuYou XinChai MengjiaWang XiaohuWang XiaoliangZhang JunmeiLiu JunjiaRen XiubaoSong WeijieQin TingtingLi SuxinWang Jian - Although immunotherapy has transformed the treatment landscape for many types of cancer, its therapeutic efficacy in glioblastoma (GBM) is limited by insufficient antigen presentation and the immunogenic cell exclusion in the tumor microenvironment. Here, we develop a candidate-based CRISPR activation (CRISPRa) functional screen to identify regulators of conventional dendritic cell (cDC)-fate specification. We determine that the transcription factors Zfp366/Znf366, Pu.1, Irf8, and Batf3 (ZPIB) are sufficient to convert GBM cells into cDC-like cells. ZPIB-mediated reprogramming results in global transcriptional and epigenetic remodeling in glioma cells. Single-cell RNA sequencing (scRNA-seq) profiling also reveals efficient and dynamic reprogramming of GBM cells to cDCs in vivo. Moreover, reprogrammed tumor cells remodel the microenvironment and elicit systemic tumor-eradicating and durable antitumor immunity in multiple mouse GBM models. Antitumor immunity elicited by ZPIB-DCs is synergistic with immune checkpoint inhibitors. Finally, we evaluate the clinical applicability of this approach by generating ZPIB-DCs from GBM patients within a humanized model. Our study represents a cellular reprogramming therapeutic strategy with broad implications for clinical immunotherapy. - Source: PubMed
Publication date: 2026/09/01
Liu XiaoZhu MaorongZou ChengCao ZhengcongWang YawenYang GuangzhaoLiu XiaolinWu YuxinYu DuoZheng DanZhang KuoLi JuanZhang WangqianWang ShuningQin HaozheHao QiangZhang YingqiYin AnanHe YalongHe LeiLuo XiaonanLin WeiLi MengGu Jintao - Mechanisms governing T cell responses to food or microbes have been characterized, but whether they also regulate gut autoimmunity is unknown. We compared ovalbumin (OVA)-specific T cell fates using mice fed OVA, or expressing secreted (s), cytosolic (c), or transmembrane (tm) epithelial OVA. At baseline and after reovirus infection, T cell responses were comparable. However, helminth infection induced T helper 2 (Th2) cell polarization in sOVA and tmOVA but not cOVA or OVA-fed mice. BATF3 antigen-presenting cells (APCs) were indispensable for CD4 T cell proliferation only in cOVA mice, yet they drove regulatory T (Treg) cell differentiation across all epithelial OVA models. In contrast, antigen presentation by RORγtMHC class II APCs was exclusively required for Treg cell induction by dietary OVA. These distinct APC dependencies correlated with susceptibility to pathology elicited by dietary versus epithelial self-antigens. Thus, antigen origin and presentation context together shape T cell fate, aiding predictions of gut immune outcomes. - Source: PubMed
Publication date: 2026/08/26
Zhou Yixuan DBrown HaileySchaffer EmilyTaylor Gwen MFiske Kay LKomnick Macy RLopez SebastianDermody Terence SEsterházy Daria