Requirement of bic/microRNA-155 for Normal Immune Function

Rodriguez, Antony; Vigorito, Elena; Clare, Simon; Warren, Madhuri V.; Couttet, Philippe; Soond, Dalya R.; van Dongen, Stijn; Grocock, Russell J.; Das, Partha P.; Miska, Eric A.; Vetrie, David; Okkenhaug, Klaus; Enright, Anton J.; Dougan, Gordon; Turner, Martin; Bradley, Allan

doi:10.1126/science.1139253

Cited by 1,833MicroRNA in disease regulationT-cell and B-cell ImmunologyImmune Response and Inflammation

Requirement of bic/microRNA-155 for Normal Immune Function

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Rodriguez, Antony, Vigorito, Elena, Clare, Simon, Warren, Madhuri V., Couttet, Philippe, Soond, Dalya R., van Dongen, Stijn, Grocock, Russell J. +8 more·2007·Science

DOI 10.1126/science.1139253PMC PMC2610435

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Abstract

MicroRNAs are a class of small RNAs that are increasingly being recognized as important regulators of gene expression. Although hundreds of microRNAs are present in the mammalian genome, genetic studies addressing their physiological roles are at an early stage. We have shown that mice deficient for bic/microRNA-155 are immunodeficient and display increased lung airway remodeling. We demonstrate a requirement of bic/microRNA-155 for the function of B and T lymphocytes and dendritic cells. Transcriptome analysis of bic/microRNA-155 –deficient CD4 + T cells identified a wide spectrum of microRNA-155–regulated genes, including cytokines, chemokines, and transcription factors. Our work suggests that bic/microRNA-155 plays a key role in the homeostasis and function of the immune system.

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Expression of miR-155 is required for normal immune function.
“Expression of miR-155 is, therefore, required for normal immune function [24].”
From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [24]

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Authors: Rodriguez, A., Vigorito, E., Clare, S., Warren, M. V., Couttet, P., Soond, D. R., van Dongen, S., Grocock, R. J., Das, P. P., Miska, E. A., Vetrie, D., Okkenhaug, K., Enright, A. J., Dougan, G., Turner, M., & Bradley, A.
Affiliations: Babraham Institute (GB)
The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.
Corresponding author: Rodriguez, Antony
Vigorito, Elena
Turner, Martin
Bradley, Allan
ORCID: Rodriguez, Antony
Vigorito, Elena
Clare, Simon
Warren, Madhuri V.
Couttet, Philippe
Das, Partha P.
Miska, Eric A.
Vetrie, David
Okkenhaug, Klaus
Enright, Anton J.
Turner, Martin
Bradley, Allan
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2007-04-27
Volume: 316
Issue: 5824
Pages: 608-611
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1139253
PMC: PMC2610435
OpenAlex: W2014869583
Cited by: 1,833
References: 29
Citations by year: 2026: 16 · 2025: 31 · 2024: 53 · 2023: 38 · 2022: 57 · 2021: 80 · 2020: 82 · 2019: 76 · 2018: 89 · 2017: 106 · 2016: 114 · 2015: 114 · 2014: 140 · 2013: 171 · 2012: 121
FWCI: 46.59
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Science (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Wellcome Trust (077187, 79643)
Biotechnology and Biological Sciences Research Council (BBS/E/B/0000M206)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: miR-155, immunodeficiency, B cells, T cells, dendritic cells, CD4+ T cells, cytokines, chemokines, transcription factors, immune homeostasis
MeSH terms: Animals, B-Lymphocytes, Dendritic Cells, Gene Expression Regulation, Homeostasis, Immunoglobulin G, Immune System, Lung, Lung Diseases, Lymphocyte Activation, Salmonella Infections, Animal, T-Lymphocytes, Vaccination, Cytokines, Gene Targeting, Th1 Cells, Th2 Cells, Oligonucleotide Array Sequence Analysis, 3' Untranslated Regions, MicroRNAs, Proto-Oncogene Proteins c-maf, Mice

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