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TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets
Dendritic cells (DCs) are professional antigen-presenting cells that sample their environment and present antigens to naïve T lymphocytes for the subsequent antigen-specific immune responses. DCs exist in a range of distinct subpopulations including plasmacytoid DCs (pDCs) and classical DCs (cDCs),...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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The Korean Association of Immunologists
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770101/ https://www.ncbi.nlm.nih.gov/pubmed/26937233 http://dx.doi.org/10.4110/in.2016.16.1.61 |
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author | Han, Sun Murray Na, Hye Young Ham, Onju Choi, Wanho Sohn, Moah Ryu, Seul Hye In, Hyunju Hwang, Ki-Chul Park, Chae Gyu |
author_facet | Han, Sun Murray Na, Hye Young Ham, Onju Choi, Wanho Sohn, Moah Ryu, Seul Hye In, Hyunju Hwang, Ki-Chul Park, Chae Gyu |
author_sort | Han, Sun Murray |
collection | PubMed |
description | Dendritic cells (DCs) are professional antigen-presenting cells that sample their environment and present antigens to naïve T lymphocytes for the subsequent antigen-specific immune responses. DCs exist in a range of distinct subpopulations including plasmacytoid DCs (pDCs) and classical DCs (cDCs), with the latter consisting of the cDC1 and cDC2 lineages. Although the roles of DC-specific transcription factors across the DC subsets have become understood, the posttranscriptional mechanisms that regulate DC development are yet to be elucidated. MicroRNAs (miRNAs) are pivotal posttranscriptional regulators of gene expression in a myriad of biological processes, but their contribution to the immune system is just beginning to surface. In this study, our in-house probe collection was screened to identify miRNAs possibly involved in DC development and function by targeting the transcripts of relevant mouse transcription factors. Examination of DC subsets from the culture of mouse bone marrow with Flt3 ligand identified high expression of miR-124 which was able to target the transcript of TCF4, a transcription factor critical for the development and homeostasis of pDCs. Further expression profiling of mouse DC subsets isolated from in vitro culture as well as via ex vivo purification demonstrated that miR-124 was outstandingly expressed in CD24(+) cDC1 cells compared to in pDCs and CD172α(+) cDC2 cells. These results imply that miR-124 is likely involved in the processes of DC subset development by posttranscriptional regulation of a transcription factor(s). |
format | Online Article Text |
id | pubmed-4770101 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | The Korean Association of Immunologists |
record_format | MEDLINE/PubMed |
spelling | pubmed-47701012016-03-02 TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets Han, Sun Murray Na, Hye Young Ham, Onju Choi, Wanho Sohn, Moah Ryu, Seul Hye In, Hyunju Hwang, Ki-Chul Park, Chae Gyu Immune Netw Original Article Dendritic cells (DCs) are professional antigen-presenting cells that sample their environment and present antigens to naïve T lymphocytes for the subsequent antigen-specific immune responses. DCs exist in a range of distinct subpopulations including plasmacytoid DCs (pDCs) and classical DCs (cDCs), with the latter consisting of the cDC1 and cDC2 lineages. Although the roles of DC-specific transcription factors across the DC subsets have become understood, the posttranscriptional mechanisms that regulate DC development are yet to be elucidated. MicroRNAs (miRNAs) are pivotal posttranscriptional regulators of gene expression in a myriad of biological processes, but their contribution to the immune system is just beginning to surface. In this study, our in-house probe collection was screened to identify miRNAs possibly involved in DC development and function by targeting the transcripts of relevant mouse transcription factors. Examination of DC subsets from the culture of mouse bone marrow with Flt3 ligand identified high expression of miR-124 which was able to target the transcript of TCF4, a transcription factor critical for the development and homeostasis of pDCs. Further expression profiling of mouse DC subsets isolated from in vitro culture as well as via ex vivo purification demonstrated that miR-124 was outstandingly expressed in CD24(+) cDC1 cells compared to in pDCs and CD172α(+) cDC2 cells. These results imply that miR-124 is likely involved in the processes of DC subset development by posttranscriptional regulation of a transcription factor(s). The Korean Association of Immunologists 2016-02 2016-02-25 /pmc/articles/PMC4770101/ /pubmed/26937233 http://dx.doi.org/10.4110/in.2016.16.1.61 Text en Copyright © 2016 The Korean Association of Immunologists http://creativecommons.org/licenses/by-nc/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Han, Sun Murray Na, Hye Young Ham, Onju Choi, Wanho Sohn, Moah Ryu, Seul Hye In, Hyunju Hwang, Ki-Chul Park, Chae Gyu TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets |
title | TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets |
title_full | TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets |
title_fullStr | TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets |
title_full_unstemmed | TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets |
title_short | TCF4-Targeting miR-124 is Differentially Expressed amongst Dendritic Cell Subsets |
title_sort | tcf4-targeting mir-124 is differentially expressed amongst dendritic cell subsets |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770101/ https://www.ncbi.nlm.nih.gov/pubmed/26937233 http://dx.doi.org/10.4110/in.2016.16.1.61 |
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