Transcriptional control of dendritic cell development.
Dendritic cells (DCs) drive both adaptive and innate immunity. Recent findings support the notion that distinct subsets of classical DCs favor alternative modules of immunity, acting on innate lymphoid-like cells (ILCs) and T cells similarly to promote either ILC1/Th1/CTL- or ILC3/Th17-type responses. Coordination between DC subsets and their favored immune module might imply that the genetic programs for DC diversification preceded the emergence of recombination-activating gene-dependent adaptive immunity and operate initially in coordinating ILC repertoires for appropriate responses against pathogens. Consequently, understanding the molecular basis of DC developmental and diversification is important for an underlying appreciation of immune regulation. Currently, the basis for DC development into the recognized subsets/lineages is only partially understood, based on the requirements for several transcription factors including PU.1, Bcl11a, Irf8, E2-2, Id2, Irf4, Irf8, Batf3, and other BATF family members. This chapter will briefly review recent transcriptional aspects of DC development and function and then highlight some currently unresolved questions.
School of Medicine, Department of Pathology and Immunology, Washington University, St. Louis, Missouri, USA; School of Medicine, Howard Hughes Medical Institute, Washington University, St. Louis, Missouri, USA. Electronic address: kmurphy@wustl.edu.
Kenneth M
KM
Murphy
D000818:Animals; D002454:Cell Differentiation; D019070:Cell Lineage; D003713:Dendritic Cells / Q000166:cytology* / Q000276:immunology / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D050835:Interferon Regulatory Factors / Q000378:metabolism; D014158:Transcription, Genetic
D050835:Interferon Regulatory Factors
Common dendritic progenitor; Dendritic cell; Lineage commitment; Transcription factors