Genetic models of human and mouse dendritic cell development and function
Dendritic cells (DCs) develop in the bone marrow from haematopoietic progenitors that have numerous shared characteristics between mice and humans. Human counterparts of mouse DC progenitors have been identified by their shared transcriptional signatures and developmental potential. New findings con...
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Published in | Nature reviews. Immunology Vol. 21; no. 2; pp. 101 - 115 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.02.2021
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
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Summary: | Dendritic cells (DCs) develop in the bone marrow from haematopoietic progenitors that have numerous shared characteristics between mice and humans. Human counterparts of mouse DC progenitors have been identified by their shared transcriptional signatures and developmental potential. New findings continue to revise models of DC ontogeny but it is well accepted that DCs can be divided into two main functional groups. Classical DCs include type 1 and type 2 subsets, which can detect different pathogens, produce specific cytokines and present antigens to polarize mainly naive CD8
+
or CD4
+
T cells, respectively. By contrast, the function of plasmacytoid DCs is largely innate and restricted to the detection of viral infections and the production of type I interferon. Here, we discuss genetic models of mouse DC development and function that have aided in correlating ontogeny with function, as well as how these findings can be translated to human DCs and their progenitors.
Genetic models of dendritic cell (DC) development in mice have aided our understanding of the redundant and non-redundant functions of DC subsets and enabled translation of these findings to human DCs. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 The authors contributed equally to all aspects of the article. Author contributions |
ISSN: | 1474-1733 1474-1741 |
DOI: | 10.1038/s41577-020-00413-x |