miRNA regulation of innate immunity

Momen-Heravi, Fatemeh; Bala, Shashi

doi:10.1002/jlb.3mir1117-459r

Cited by 88 publications

(77 citation statements)

References 146 publications

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“…MicroRNAs are evolutionarily conserved noncoding RNA oligonucleotides and are involved in the pathology of numerous diseases. 26,27 According to previous studies, miR-124, miR-125a, and miR-146b, which are frequently investigated miRNAs, are well known as inflammation-related miRNAs, moreover, they have been identified as direct target genes of lncRNA NEAT1. [18][19][20] Thus, we hypothesized that lncRNA NEAT1 might function via regulating miR-124, miR-125a, and miR-146b in AIS as well.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1 correlates with higher disease risk, worse disease condition, decreased miR‐124 and miR‐125a and predicts poor recurrence‐free survival of acute ischemic stroke

Duan

2019

Clinical Laboratory Analysis

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Objective This study aimed to investigate the predictive value of long noncoding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) for acute ischemic stroke (AIS) risk and to explore the correlation of lncRNA NEAT1 with disease severity, inflammation, recurrence and target microRNAs in patients with AIS. Methods 210 patients with AIS and 210 controls were enrolled, and their peripheral blood samples were collected within 24 hours after admission and collected on the enrollment, respectively. lncRNA NEAT1 expression was detected by quantitative polymerase chain reaction (qPCR). For patients with AIS, disease severity was evaluated by National Institute of Health Stroke Scale (NIHSS) score; plasma concentrations of inflammatory factors and lncRNA NEAT1 target microRNAs were measured by enzyme‐linked immune sorbent assay and qPCR, respectively; stroke recurrence and death were recorded; and recurrence‐free survival (RFS) was calculated. Results lncRNA NEAT1 expression was elevated in patients with AIS compared with controls, and it had a good predictive value for AIS risk (area under the curve [AUC]: 0.804 [95% confidence interval [CI]: 0.763‐0.845]). In patients with AIS, lncRNA NEAT1 expression positively correlated with NIHSS score and inflammatory factor levels including C‐reactive protein (CRP), tumor necrosis factor (TNF)‐α, interleukin (IL)‐6, IL‐8, and IL‐22, while it negatively correlated with anti‐inflammatory cytokine IL‐10 level. Besides, lncRNA NEAT1 predicted increased recurrence/death risk (AUC: 0.641 [95% CI: 0.541‐0.741]), and its high expression correlated with worse RFS. Additionally, lncRNA NEAT1 expression negatively correlated with microRNA‐124 and microRNA‐125a expressions. Conclusion LncRNA NEAT1 may serve as a novel biomarker for assisting AIS management and prognosis.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA NEAT1 correlates with higher disease risk, worse disease condition, decreased miR‐124 and miR‐125a and predicts poor recurrence‐free survival of acute ischemic stroke

Duan

2019

Clinical Laboratory Analysis

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“…They are expressed by various innate immune cells, such as monocytes, macrophages, DCs, granulocytes, and NK cells. miRNAs are crucial in the development and function of innate immune cells and play a role in adaptive immune cell regulation . Dysfunction of miRNAs can induce inflammatory diseases and autoimmunity .…”

Section: The Role Of the Innate Immune System During The Early Stagesmentioning

confidence: 99%

“…miRNAs are crucial in the development and function of innate immune cells and play a role in adaptive immune cell regulation. 188,189 Dysfunction of miRNAs can induce inflammatory diseases and autoimmunity. 190 In mouse studies, several miRNAs are reported to modulate experimental models of arthritis, including miR- 155, 191 miR-223, 192 and miR-146a.…”

Section: Inhibition Of Myostatin In Vivo Suppressed Lyme Arthritis Inmentioning

confidence: 99%

A joint effort: The interplay between the innate and the adaptive immune system in Lyme arthritis

Brouwer

Schoor

Vrijmoeth

et al. 2020

Immunological Reviews

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Articular joints are a major target of Borrelia burgdorferi, the causative agent of Lyme arthritis. Despite antibiotic treatment, recurrent or persistent Lyme arthritis is observed in a significant number of patients. The host immune response plays a crucial role in this chronic arthritic joint complication of Borrelia infections. During the early stages of B. burgdorferi infection, a major hinder in generating a proper host immune response is the lack of induction of a strong adaptive immune response. This may lead to a delayed hyperinflammatory reaction later in the disease. Several mechanisms have been suggested that might be pivotal for the development of Lyme arthritis and will be highlighted in this review, from molecular mimicry of matrix metallopeptidases and glycosaminoglycans, to autoimmune responses to live bacteria, or remnants of Borrelia spirochetes in joints. Murine studies have suggested that the inflammatory responses are initiated by innate immune cells, but this does not exclude the involvement of the adaptive immune system in this dysregulated immune profile. Genetic predisposition, via human leukocyte antigen‐DR isotype and microRNA expression, has been associated with the development of antibiotic‐refractory Lyme arthritis. Yet the ultimate cause for (antibiotic‐refractory) Lyme arthritis remains unknown. Complex processes of different immune cells and signaling cascades are involved in the development of Lyme arthritis. When these various mechanisms are fully been unraveled, new treatment strategies can be developed to target (antibiotic‐refractory) Lyme arthritis more effectively.

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“…In this case, the effects are due to the intercellular exchange of specific membrane and cargo molecules [7][8][9][10][11][12]. A third mechanism recognized now is due to EVs released from, and then fused to, target cells.…”

Section: Physiological Ev Effects In Immunologymentioning

confidence: 99%

“…When transferred to the cytoplasm of immune target cells these RNAs govern various processes, including expression of immune genes and proteins relevant for development and function [12,14]. When transferred to the cytoplasm of immune target cells these RNAs govern various processes, including expression of immune genes and proteins relevant for development and function [12,14].…”

Section: Physiological Ev Effects In Immunologymentioning

confidence: 99%

Extracellular vesicles, news about their role in immune cells: physiology, pathology and diseases

Meldolesi

2019

Clinical and Experimental Immunology

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Two types of extracellular vesicles (EVs), exosomes and ectosomes, are generated and released by all cells, including immune cells. The two EVs appear different in many properties: size, mechanism and site of assembly, composition of their membranes and luminal cargoes, sites and processes of release. In functional terms, however, these differences are minor. Moreover, their binding to and effects on target cells appear similar, thus the two types are considered distinct only in a few cases, otherwise they are presented together as EVs. The EV physiology of the various immune cells differs as expected from their differential properties. Some properties, however, are common: EV release, taking place already at rest, is greatly increased upon cell stimulation; extracellular navigation occurs adjacent and at distance from the releasing cells; binding to and uptake by target cells are specific. EVs received from other immune or distinct cells govern many functions in target cells. Immune diseases in which EVs play multiple, often opposite (aggression and protection) effects, are numerous; inflammatory diseases; pathologies of various tissues; and brain diseases, such as multiple sclerosis. EVs also have effects on interactive immune and cancer cells. These effects are often distinct, promoting cytotoxicity or proliferation, the latter together with metastasis and angiogenesis. Diagnoses depend on the identification of EV biomarkers; therapies on various mechanisms such as (1) removal of aggression-inducing EVs; (2) EV manipulations specific for single targets, with insertion of surface peptides or luminal miRNAs; and (3) removal or re-expression of molecules from target cells.

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miRNA regulation of innate immunity

Cited by 88 publications

References 146 publications

Long noncoding RNA NEAT1 correlates with higher disease risk, worse disease condition, decreased miR‐124 and miR‐125a and predicts poor recurrence‐free survival of acute ischemic stroke

Long noncoding RNA NEAT1 correlates with higher disease risk, worse disease condition, decreased miR‐124 and miR‐125a and predicts poor recurrence‐free survival of acute ischemic stroke

A joint effort: The interplay between the innate and the adaptive immune system in Lyme arthritis

Extracellular vesicles, news about their role in immune cells: physiology, pathology and diseases

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