MicroRNA regulation of innate immune responses in epithelial cells

Rui Zhou, Steven P. O'Hara, Xian-Ming Chen

Research output: Contribution to journalReview article

73 Citations (Scopus)

Abstract

Mucosal surface epithelial cells are equipped with several defense mechanisms that guard against pathogens. Recent studies indicate that microRNAs (miRNAs) mediate post-transcriptional gene suppression and may be a critical component of the complex regulatory networks in epithelial immune responses. Transcription of miRNA genes in epithelial cells can be elaborately controlled through pathogen recognition receptors, such as Toll-like receptors (TLRs), and associated nuclear factor kappaB (NF-β °B) and mitogen-activated protein kinase (MAPK) pathways, and ultimately nuclear transcription factor associated-transactivation and transrepression. Activation of these intracellular signaling pathways may also modulate the process of miRNA maturation. Functionally, miRNAs may modulate epithelial immune responses at every step of the innate immune network, including production and release of cytokines/chemokines, expression of adhesion and costimulatory molecules, shuttling of miRNAs through release of exosomes and feedback regulation of immune homeostasis. Therefore, miRNAs act as critical regulators to the fine-tuning of epithelial immune responses.

Original languageEnglish
Pages (from-to)371-379
Number of pages9
JournalCellular and Molecular Immunology
Volume8
Issue number5
DOIs
StatePublished - Sep 2011

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MicroRNAs
Innate Immunity
Epithelial Cells
Exosomes
Toll-Like Receptors
Mitogen-Activated Protein Kinases
Chemokines
Transcriptional Activation
Genes
Homeostasis
Transcription Factors
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

Cite this

MicroRNA regulation of innate immune responses in epithelial cells. / Zhou, Rui; O'Hara, Steven P.; Chen, Xian-Ming.

In: Cellular and Molecular Immunology, Vol. 8, No. 5, 09.2011, p. 371-379.

Research output: Contribution to journalReview article

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