Batf3 selectively determines acquisition of CD8+ dendritic cell phenotype and function

Chandra, Janin, Kuo, Paula T. Y., Hahn, Anne M., Belz, Gabrielle T. and Frazer, Ian H. (2016) Batf3 selectively determines acquisition of CD8+ dendritic cell phenotype and function. Immunology and Cell Biology, 95 2: 215-223. doi:10.1038/icb.2016.83


Author Chandra, Janin
Kuo, Paula T. Y.
Hahn, Anne M.
Belz, Gabrielle T.
Frazer, Ian H.
Title Batf3 selectively determines acquisition of CD8+ dendritic cell phenotype and function
Formatted title
Batf3 selectively determines acquisition of CD8+ dendritic cell phenotype and function
Journal name Immunology and Cell Biology   Check publisher's open access policy
ISSN 0818-9641
1440-1711
Publication date 2016-11-29
Year available 2017
Sub-type Letter to editor, brief commentary or brief communication
DOI 10.1038/icb.2016.83
Open Access Status Not yet assessed
Volume 95
Issue 2
Start page 215
End page 223
Total pages 9
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Language eng
Subject 2403 Immunology
1307 Cell Biology
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 CD172α, 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.
Formatted 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 CD172α, 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.
Keyword Cell Biology
Immunology
Cell Biology
Immunology
Q-Index Code CX
Q-Index Status Provisional Code
Grant ID P01 CA022443
Institutional Status UQ

Document type: Journal Article
Sub-type: Letter to editor, brief commentary or brief communication
Collections: HERDC Pre-Audit
UQ Diamantina Institute Publications
 
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