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Expression data from DC1 purified from spleens of WT, WT Irf8VENUS+, and Batf3-/- Irf8VENUS+ mice.

ABSTRACT: Batf3-/- mice have impaired development of DC1 . However, DC1 development is restored in Batf3-/- mice containing an Irf8VENUS transgene. Even though DC1 development was restored in these mice, they were still unable to reject a transplanted immunogenic fibrosarcoma, indicating that there are some functions of Batf3-dependent dendritic cells that are not restored by the Irf8VENUS transgene.

ORGANISM(S): Mus musculus

PROVIDER: GSE111034 | GEO | 2018/11/30

REPOSITORIES: GEO

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Expression data from DC1 purified from spleens of WT, WT Irf8VENUS+, and Batf3-/- Irf8VENUS+ mice.

Project description:Expression data from DC1 purified from spleens of WT, WT Irf8VENUS+, and Batf3-/- Irf8VENUS+ mice.

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Batf3 maintains Irf8 autoactivation for commitment of a novel clonogenic progenitor of CD8+DCs

Project description:The transcription factors Batf3 and IRF8 are required for development of CD8α+ conventional dendritic cells (cDCs), but the basis for their actions was unclear. Here, we identify two novel Zbtb46+ progenitors that separately generate CD8α+ and CD4+ cDCs and arise directly from the common DC progenitor (CDP). Irf8 expression in the CDP depends on prior PU.1-dependent autoactivation, and specification of pre-CD8 DC progenitors requires IRF8 but not Batf3. However, upon pre-CD8 DC specification, Irf8 autoactivation becomes Batf3-dependent at a CD8α+ cDC-specific enhancer containing multiple AP1-IRF composite elements (AICEs) within the Irf8 superenhancer. CDPs from Batf3-/- mice that specify toward pre-CD8 DCs fail to complete CD8α+ cDC development due to decay of Irf8 autoactivation, and divert to the CD4+ cDC lineage. Examination of histone modifications (H3K27ac and H3K4me1) and 2 transcription factors (Batf3 and Irf8) and the p300 co-factor binding in 3 different dendritic cell subsets

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Project description:Anti-viral CD8 T cell responses are characterized by an initial activation/priming of T lymphocytes followed by a massive proliferation, subset differentiation, population contraction and the development of a stable memory pool. The transcription factor BATF3 has been shown to play a central role in the development of conventional dendritic cells (cDC1), which in turn are critical for the optimal priming of CD8 T cells. Here we show that BATF3 is expressed within the first days after priming but has long-lasting T cell intrinsic effects. We found that T cells that lack Batf3 show a normal expansion and differentiation, yet succumbed to an aggravated contraction and had a diminished memory response. Vice versa BATF3-overexpression in CD8 T cells promoted their survival and transition to memory. Mechanistically, BATF3 regulates T cell apoptosis and longevity via the proapoptotic factor BIM. By programing CD8 T cell survival and memory, BATF3 is a promising molecule to optimize adoptive T cell therapy in patients.

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Enterobacter sp. DC1

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Microarray analysis of WT and Batf3-/- CD8alpha dendritic cells from C57BL/6 spleen

Project description:Batf3 regulates key CD8alpha DC-specific genes.

2012-09-30 | GSE40647 | GEO

Microarray analysis of WT and Batf3-/- CD8alpha dendritic cells from C57BL/6 spleen

Project description:Batf3 regulates key CD8alpha DC-specific genes. WT and KO cells were isolated from pooled spleens of C57BL/6 genetic background mice, that were either untreated, or injected with recombinant murine IL-12 in pyrogen-free saline at 2.5 ug/mL. Mice were injected i.p. with 0.5 ug of IL-12 once and sorted after 3 days. CD8alpha+ dendritic cells were sorted as B220- NK1.1- CD172a- CD11c+ MHCII+ CD24+ DEC205+ CD8alpha+ cells.

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BATF3-dependent IRF4 binding inhibits FOXP3 in differentiating Tregs

Project description:BATF3 has been shown to inhibit FOXP3 expression in differentiating CD4 T cells, however, the role of IRF4 in this inhibition is unexplored. IRF4 binds DNA weakly on its own and requires interactions with other transcription factors. We investigated how BATF3/IRF4 interactions are necessary for IRF4 binding and BATF3-mediated FOXP3 inhibition.

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