MicroRNA‐590‐3p inhibits T helper 17 cells and ameliorates inflammation in lupus mice

Huang, Jiuzuo; Xu, Xinzhi; Wang, Xiuyuan; Yang, Jie; Xue, Meijuan; Yang, Yiming; Zhang, Ruomei; Yang, Xue; Yang, Ji

doi:10.1111/imm.13434

Cited by 18 publications

(12 citation statements)

References 49 publications

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“…An et al reported that the administration of autophagic inhibitor hydroxychloroquine to MRL/lpr mice, which spontaneously develop SLE-like inflammation, ameliorates SLE-induced nephritis pathology, such as mesangial cellular proliferation ( An et al, 2017 ). Consistent with this finding, the administration of an microRNA-590-3p agomir to MRL/lpr mice attenuated the pathology score of lupus nephritis ( Huang et al, 2021 ). In a murine autoimmune myocarditis model, the administration of bazedoxifene reduced Th17 differentiation, resulting in improved myocarditis pathology ( Wang et al, 2021 ).…”

Section: Cd4 + T Differentiationsupporting

confidence: 58%

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The Role of Autophagy in the Function of CD4+ T Cells and the Development of Chronic Inflammatory Diseases

2022

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Uncontrolled acute inflammation progresses to persistent inflammation that leads to various chronic inflammatory diseases, including asthma, Crohn’s disease, rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus. CD4+ T cells are key immune cells that determine the development of these chronic inflammatory diseases. CD4+ T cells orchestrate adaptive immune responses by producing cytokines and effector molecules. These functional roles of T cells vary depending on the surrounding inflammatory or anatomical environment. Autophagy is an important process that can regulate the function of CD4+ T cells. By lysosomal degradation of cytoplasmic materials, autophagy mediates CD4+ T cell-mediated immune responses, including cytokine production, proliferation, and differentiation. Furthermore, through canonical processes involving autophagy machinery, autophagy also contributes to the development of chronic inflammatory diseases. Therefore, a targeted intervention of autophagy processes could be used to treat chronic inflammatory diseases. This review focuses on the role of autophagy via CD4+ T cells in the pathogenesis and treatment of such diseases. In particular, we explore the underlying mechanisms of autophagy in the regulation of CD4+ T cell metabolism, survival, development, proliferation, differentiation, and aging. Furthermore, we suggest that autophagy-mediated modulation of CD4+ T cells is a promising therapeutic target for treating chronic inflammatory diseases.

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Section: Cd4 + T Differentiationsupporting

confidence: 58%

“…Similar to Th1 cells, autophagy-deficient Th17 cells are susceptible to cell death. According to Huang et al, autophagy-deficient human CD4 + T cells overexpressing microRNA-590-3p showed reduction of Th17 differentiation by increased apoptosis ( Huang et al, 2021 ).…”

Section: Cd4 + T Differentiationmentioning

confidence: 99%

The Role of Autophagy in the Function of CD4+ T Cells and the Development of Chronic Inflammatory Diseases

2022

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“…A recent study suggested that miR-590-3p can suppress Th17 cells by inhibiting autophagy; increasing miR-590-3p expression can improve lupus nephritis and skin injury in MRL/lpr mice, providing a possible direction for the treatment of SLE symptoms. 36 The organ most severely damaged by inflammation in SLE is the kidney. MiR-146a reduces kidney injury in MRL/lpr mice by inhibiting the expression of TRAF6 and IRAK1 target genes and contributes to LN treatment.…”

Section: Mirnas and The Diagnosis Of Sle And Lnmentioning

confidence: 99%

Advances in the study of exosome-derived miRNAs in the pathogenesis, diagnosis, and treatment of systemic lupus erythematosus

Wu,

Dong,

Liu

et al. 2023

Lupus

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Systemic lupus erythematosus (SLE) is an inflammatory disease caused by autoantibodies, with high morbidity and mortality. It involves multiple systems, particularly the renal, which can lead to lupus nephritis (LN); its multi-system effects have a significant impact on the physical and mental health of patients. Exosomes are vesicles that are secreted during cell activity and carry a variety of nucleic acids, proteins, and lipids. They are distributed through body fluids for cellular communication. MicroRNAs (miRNAs) are nucleic acids that are packaged within the exosome that are taken up and released in response to changes in plasma membrane structure. MiRNAs are potential participants in immune and inflammatory responses, which are transported to target cells and can inhibit gene expression in receptor cells. It has been suggested that exosomal miRNA can regulate the pathogenesis of SLE and, as such, they are of value in diagnosis and treatment. In this paper, we focus on the research progress into exosomal miRNA in SLE and inspire new directions for SLE related research.

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“…Lupus erythematosus lesions in the skin share extensive lymphocyte infiltration with a high predominance of CD4 T cells and cytokines, including TNF-α, IL-1α, IL-1β, IL-6, and IL-8 [ 114 ]. Huang et al [ 115 ] found a correlation between the increase in Th17 cells and the decrease in miR-590-3p in systemic lupus erythematosus patients and MRL/lpr mice. miR-590-3p agomir transfection promoted the apoptosis of Th17 cells by autophagy suppression via direct targeting of autophagy-related 7 (Atg7).…”

Section: Mirnas For Treating Inflammatory Skin Diseasesmentioning

confidence: 99%

Anti-Inflammatory microRNAs for Treating Inflammatory Skin Diseases

et al. 2022

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Skin inflammation occurs due to immune dysregulation because of internal disorders, infections, and allergic reactions. The inflammation of the skin is a major sign of chronic autoimmune inflammatory diseases, such as psoriasis, atopic dermatitis (AD), and lupus erythematosus. Although there are many therapies for treating these cutaneous inflammation diseases, their recurrence rates are high due to incomplete resolution. MicroRNA (miRNA) plays a critical role in skin inflammation by regulating the expression of protein-coding genes at the posttranscriptional level during pathogenesis and homeostasis maintenance. Some miRNAs possess anti-inflammatory features, which are beneficial for mitigating the inflammatory response. miRNAs that are reduced in inflammatory skin diseases can be supplied transiently using miRNA mimics and agomir. miRNA-based therapies that can target multiple genes in a given pathway are potential candidates for the treatment of skin inflammation. This review article offers an overview of the function of miRNA in skin inflammation regulation, with a focus on psoriasis, AD, and cutaneous wounds. Some bioactive molecules can target and modulate miRNAs to achieve the objective of inflammation suppression. This review also reports the anti-inflammatory efficacy of these molecules through modulating miRNA expression. The main limitations of miRNA-based therapies are rapid biodegradation and poor skin and cell penetration. Consideration was given to improving these drawbacks using the approaches of cell-penetrating peptides (CPPs), nanocarriers, exosomes, and low-frequency ultrasound. A formulation design for successful miRNA delivery into skin and target cells is also described in this review. The possible use of miRNAs as biomarkers and therapeutic modalities could open a novel opportunity for the diagnosis and treatment of inflammation-associated skin diseases.

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MicroRNA‐590‐3p inhibits T helper 17 cells and ameliorates inflammation in lupus mice

Cited by 18 publications

References 49 publications

The Role of Autophagy in the Function of CD4+ T Cells and the Development of Chronic Inflammatory Diseases

The Role of Autophagy in the Function of CD4+ T Cells and the Development of Chronic Inflammatory Diseases

Advances in the study of exosome-derived miRNAs in the pathogenesis, diagnosis, and treatment of systemic lupus erythematosus

Anti-Inflammatory microRNAs for Treating Inflammatory Skin Diseases

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