Batf3 selectively determines acquisition of CD8+ dendritic cell phenotype and function
- Author(s)
- Chandra, J; Kuo, PT; Hahn, AM; Belz, GT; Frazer, IH;
- Details
- Publication Year 2017-11-29,Volume 95,Issue #2,Page 215-223
- Journal Title
- Immunol Cell Biol
- Publication Type
- Journal Article
- Abstract
- Batf3 is a transcription factor that impacts the development of CD103+ tissue-resident dendritic cells (DCs). However, whether Batf3 is absolutely required for the development of CD8+ DCs remains controversial. Id2 is required for CD8+ DC development. Here we show that bone marrow chimeric mice with a deletion of Id2 in the CD11c compartment lose the ability to reject a skin graft expressing a non-self protein antigen or mount a delayed hypersensitivity response. In contrast, Batf3-/- mice remained competent for skin graft rejection and delayed hypersensitivity, and retained a CD8+ DC population with markers characteristic of the CD11b+ DC lineage, including CD11b, CD4 and CD172alpha, as well as the key regulator transcription factor IRF4, but lacked IRF8 expression. CD8+ DCs in Batf3-/- mice took up and cleaved protein antigen and larger particles but were unable to phagocytose dying cells, a characteristic feature to the CD8+ DC lineage. These data clarify a requirement for CD8+ lineage DCs to induce effectors of neo-antigen-driven skin graft rejection, and improve our understanding of DC subtype commitment by demonstrating that in the absence of Batf3 CD8+ DCs can change their fate and become CD11b+ DCs.Immunology and Cell Biology advance online publication, 29 November 2016; doi:10.1038/icb.2016.83.
- Publisher
- Springer Nature
- Research Division(s)
- Molecular Immunology
- PubMed ID
- 27897162
- Publisher's Version
- https://doi.org/10.1038/icb.2016.83
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2017-05-26 03:11:42
Last Modified: 2017-05-26 03:31:24