title: microRNA miR-17-92 cluster is highly expressed in epidermal Langerhans cells but not required for its development.
abstract: Langerhans cells (LCs) are bone marrow-derived immature skin-residential dendritic cells (DCs) with a life cycle distinct from that of other types of DCs. The mechanisms involved in LC homeostasis and immunological functions are still not clear. MicroRNAs (miRNAs) are a class of short noncoding RNAs that regulate gene expression through either translational repression or mRNA degradation. A recent study showed that specific deletion of total miRNAs in DCs affects the homeostasis and function of only LCs, but not of other types of DCs. The roles of specific individual miRNA in LC development are still lacking. The miRNA miR-17-92 class, encoding miR-17, miR-18, miR-19a, miR-19b, miR-20 and miR-92, plays a very important role in B- and T-cell development and function. Here, we first report that epidermal LCs highly express the miR-17-92 class compared with spleen naive T cells. To further characterize the role of miR-17-92 in LC development, we generated LC-specific miR-17-92 knockout and knock-in mice. Interestingly, LC-specific gain- and loss-of-function of miR-17-92 cluster did not significantly change LC homeostasis, maturation ability, antigen capture and migration to draining lymph nodes. Thus, the miR-17-92 cluster may be functionally redundant and not critically required for LC development and function.
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA [3] Department of Internal Medicine, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: L
authors.initials: L
authors.lastname: Zhou
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: R-Q
authors.initials: RQ
authors.lastname: Qi
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: M
authors.initials: M
authors.lastname: Liu
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: Y-P
authors.initials: YP
authors.lastname: Xu
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: G
authors.initials: G
authors.lastname: Li
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: M
authors.initials: M
authors.lastname: Weiland
authors.affiliation: Department of Dermatology and Center for Immunology, University of Minnesota, Minneapolis, MN, USA.
authors.forename: D H
authors.initials: DH
authors.lastname: Kaplan
authors.affiliation: 1] Henry Ford Immunology Program, Henry Ford Hospital, Detroit, MI, USA [2] Department of Dermatology, Henry Ford Hospital, Detroit, MI, USA [3] Department of Internal Medicine, Henry Ford Hospital, Detroit, MI, USA.
authors.forename: Q-S
authors.initials: QS
authors.lastname: Mi
mesh_terms: D000818:Animals; D002465:Cell Movement; D017449:Dermatitis, Allergic Contact / Q000235:genetics / Q000276:immunology; D004139:Dinitrofluorobenzene / Q000276:immunology / Q000633:toxicity; D000078404:Epidermal Cells; D005786:Gene Expression Regulation; D006706:Homeostasis; D007801:Langerhans Cells / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D035683:MicroRNAs / Q000235:genetics*; D005810:Multigene Family; D013154:Spleen / Q000166:cytology; D013601:T-Lymphocytes / Q000502:physiology
chemical_list: C575895:MIRN17-92 microRNA, mouse; D035683:MicroRNAs; D004139:Dinitrofluorobenzene