Granulocytic myeloid-derived suppressor cells contribute to IFN-I signaling activation of B cells and disease progression through the lncRNA NEAT1-BAFF axis in systemic lupus erythematosus

Dong, Guanjun; Yang, Yonghong; Li, Xuehui; Yao, Xiaoying; Zhu, Ye; Zhang, Hui; Wang, Haiyan; Ma, Qun; Zhang, Junfeng; Shi, Hui; Ning, Zhaochen; Yan, Fenglian; Zhai, Weiwei; Dai, Jun; Li, Zhihua; Li, Chunxia; Ming, Jian; Xue, Qiao; Meng, Xiangzhi; Si, Chuanping; Xiong, Huabao

doi:10.1016/j.bbadis.2019.165554

Cited by 46 publications

(38 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IFN-I not only directly mobilized BAFF (133,134) but also indirectly regulated the BAFF pathway by promoting the production of macrophage inhibitory factor (MIF) (146)(147)(148). BAFF also promotes the activation of B cells by IFN (149). Besides, SLE-related autoantibodies and ICs can induce the strong release of NETs ( 150), increasing nucleic acid exposure.…”

Section: Ifn-i Promotes the Formation Of Nuclear Antigens And Autoantibodiesmentioning

confidence: 99%

IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis

Ding

Ren

2021

Front. Immunol.

View full text Add to dashboard Cite

Lupus nephritis (LN) is a common complication of systemic lupus erythematosus (SLE) and a major risk factor for morbidity and mortality. The abundant cell-free nucleic (DNA/RNA) in SLE patients, especially dsDNA, is a key substance in the pathogenesis of SLE and LN. The deposition of DNA/RNA-immune complexes (DNA/RNA-ICs) in the glomerulus causes a series of inflammatory reactions that lead to resident renal cell disturbance and eventually renal fibrosis. Cell-free DNA/RNA is the most effective inducer of type I interferons (IFN-I). Resident renal cells (rather than infiltrating immune cells) are the main source of IFN-I in the kidney. IFN-I in turn damages resident renal cells. Not only are resident renal cells victims, but also participants in this immunity war. However, the mechanism for generation of IFN-I in resident renal cells and the pathological mechanism of IFN-I promoting renal fibrosis have not been fully elucidated. This paper reviews the latest epidemiology of LN and its development process, discusses the mechanism for generation of IFN-I in resident renal cells and the role of IFN-I in the pathogenesis of LN, and may open a new perspective for the treatment of LN.

show abstract

Section: Ifn-i Promotes the Formation Of Nuclear Antigens And Autoantibodiesmentioning

confidence: 99%

IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis

Ding

Ren

2021

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…Further in vitro studies proved that NEAT1 regulates LPS-induced expression of IL-6, CCL2, and CXCL10, which play critical roles in the pathogenesis of SLE by recruiting inflammatory cells through the regulation of the MAPK signaling pathways [ 98 ]. A recent study demonstrated that the lncRNA NEAT1-BAFF axis contributes to the activation of B cells and disease progression in SLE [ 99 ].…”

Section: Important Roles Of Lncrnas In Autoimmune Diseasesmentioning

confidence: 99%

Involvement of long noncoding RNAs in the pathogenesis of autoimmune diseases

Zou

2020

Journal of Translational Autoimmunity

View full text Add to dashboard Cite

Autoimmune diseases are a group of heterogeneous disorders characterized by damage to various organs caused by abnormal innate and adaptive immune responses. The pathogenesis of autoimmune diseases is extremely complicated and has not yet been fully elucidated. Long noncoding RNAs (lncRNAs), which are defined as transcripts containing more than 200 nucleotides with no protein-coding capacity, are emerging as important regulators of gene expression via epigenetic modification, transcriptional regulation and posttranscriptional regulation. Accumulating evidence has demonstrated that lncRNAs play a key role in the regulation of immunological functions and autoimmunity. In this review, we discuss various molecular mechanisms by which lncRNAs regulate gene expression and recent findings regarding the involvement of lncRNAs in many human autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), idiopathic inflammatory myopathy (IIM), systemic sclerosis (SSc) and Sjögren’s syndrome (pSS).

show abstract

“…Instead, NEAT1 is a global regulator that directly impacts innate immune activation during viral sensing and downstream events. Thus, NEAT1 depletion increases the replication of several viruses, including HIV and HSV, and decreases lupus symptoms in mice [133][134][135]. Recently, it was shown that NEAT1 was induced by Hantaan virus (HTNV) through the RIG-I-IRF7 pathway in a time-and dose-dependent manner and promoted HTNV-induced IFN production by facilitating RIG-I and DDX60 expression [136].…”

Section: Lncrnas Can Modulate the Levels Of Nucleic-acid Sensorsmentioning

confidence: 99%

LncRNAs in the Type I Interferon Antiviral Response

Suarez

Prats-Mari

Unfried

et al. 2020

IJMS

View full text Add to dashboard Cite

The proper functioning of the immune system requires a robust control over a delicate equilibrium between an ineffective response and immune overactivation. Poor responses to viral insults may lead to chronic or overwhelming infection, whereas unrestrained activation can cause autoimmune diseases and cancer. Control over the magnitude and duration of the antiviral immune response is exerted by a finely tuned positive or negative regulation at the DNA, RNA, and protein level of members of the type I interferon (IFN) signaling pathways and on the expression and activity of antiviral and proinflammatory factors. As summarized in this review, committed research during the last decade has shown that several of these processes are exquisitely regulated by long non-coding RNAs (lncRNAs), transcripts with poor coding capacity, but highly versatile functions. After infection, viruses, and the antiviral response they trigger, deregulate the expression of a subset of specific lncRNAs that function to promote or repress viral replication by inactivating or potentiating the antiviral response, respectively. These IFN-related lncRNAs are also highly tissue- and cell-type-specific, rendering them as promising biomarkers or therapeutic candidates to modulate specific stages of the antiviral immune response with fewer adverse effects.

show abstract

Granulocytic myeloid-derived suppressor cells contribute to IFN-I signaling activation of B cells and disease progression through the lncRNA NEAT1-BAFF axis in systemic lupus erythematosus

Cited by 46 publications

References 43 publications

IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis

IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis

Involvement of long noncoding RNAs in the pathogenesis of autoimmune diseases

LncRNAs in the Type I Interferon Antiviral Response

Contact Info

Product

Resources

About