A review of advances in the understanding of lupus nephritis pathogenesis as a basis for emerging therapies

Yung, Susan; Yap, Desmond Y H; Chan, Tak Mao

doi:10.12688/f1000research.22438.1

Cited by 21 publications

(16 citation statements)

References 133 publications

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“…SLE is a chronic autoimmune disease that is characterized by multiple autoantibodies and involves both the innate and adaptive immune systems (36). LN is a common clinical presentation of SLE (3)(4)(5), and its pathogenesis includes autoantibody production, abnormal activation of innate and adaptive immune responses, and immune-mediated renal injury (37). Early studies on the pathogenesis of LN focused on the adaptive immune system.…”

Section: Discussionmentioning

confidence: 99%

GBP2 acts as a member of the interferon signaling pathway in lupus nephritis

Zhang

Liao

Hang

et al. 2022

Preprint

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Lupus nephritis (LN) is a common and serious clinical manifestation of systemic lupus erythematosus (SLE). However, the pathogenesis of LN is not fully understood. The currently available treatments do not cure the disease and appear to have a variety of side effects in the long term. The purpose of this study was to search for key molecules involved in the immune response during the development of LN through bioinformatics techniques to provide a reference for LN-specific targeted therapy. The GSE112943 dataset was downloaded from the Gene Expression Omnibus (GEO) database, and 20 of the samples were selected for analysis. In, total 2330 differentially expressed genes were screened. These differentially expressed genes were intersected with a list of immune genes obtained from the IMMPORT immune database to obtain a total of 128 differentially expressed immune-related genes. Enrichment analysis showed that most of these genes were enriched in the interferon (IFN) signaling pathway. Gene set enrichment analysis (GSEA) revealed that the overall expression information of the sample was also significantly enriched in the interferon signaling pathway. Further analysis of the core gene cluster showed that nine genes, GBP2, VCAM1, ADAR, IFITM1, BST2, MX2, IRF5, OAS1 and TRIM22, were involved in the interferon signaling pathway. According to our analysis, the guanylate binding protein 2 (GBP2), interferon regulatory factor 5 (IRF5) and 2'-5'-oligoadenylate synthetase 1 (OAS1) genes are involved in three interferon signaling pathways. At present, we do not know whether GBP2 is associated with LN. Therefore, this study focuses on the relationship between GBP2 and LN pathogenesis. We speculate that GBP2 may play a role in the pathogenesis of LN as a member of the interferon signaling pathway. Further immunohistochemical results showed that the expression of GBP2 was increased in the renal tissues of LN patients compared with the control group, confirming this conjecture. In conclusion, according to our study, GBP2 is a member of the interferon signaling pathway that may have implications for the pathogenesis of LN and serves as a potential biomarker for LN.

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Section: Discussionmentioning

confidence: 99%

GBP2 acts as a member of the interferon signaling pathway in lupus nephritis

Zhang

Liao

Hang

et al. 2022

Preprint

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“…SLE is a chronic autoimmune disease that is characterized by multiple autoantibodies and involves both the innate and adaptive immune systems [27]. LN is a common clinical presentation of SLE [3][4][5], and its pathogenesis includes autoantibody production, abnormal activation of innate and adaptive immune responses, and immune-mediated renal injury [28]. Early studies on the pathogenesis of LN focused on the adaptive immune system.…”

Section: Discussionmentioning

confidence: 99%

GBP2 acts as a member of the interferon signalling pathway in lupus nephritis

et al. 2022

View full text Add to dashboard Cite

Lupus nephritis (LN) is a common and serious clinical manifestation of systemic lupus erythematosus. However, the pathogenesis of LN is not fully understood. The currently available treatments do not cure the disease and appear to have a variety of side effects in the long term. The purpose of this study was to search for key molecules involved in the LN immune response through bioinformatics techniques to provide a reference for LN-specific targeted therapy. The GSE112943 dataset was downloaded from the Gene Expression Omnibus database, and 20 of the samples were selected for analysis. In total, 2330 differentially expressed genes were screened. These genes were intersected with a list of immune genes obtained from the IMMPORT immune database to obtain 128 differentially expressed immune-related genes. Enrichment analysis showed that most of these genes were enriched in the interferon signalling pathway. Gene set enrichment analysis revealed that the sample was significantly enriched for expression of the interferon signalling pathway. Further analysis of the core gene cluster showed that nine genes, GBP2, VCAM1, ADAR, IFITM1, BST2, MX2, IRF5, OAS1 and TRIM22, were involved in the interferon signalling pathway. According to our analysis, the guanylate binding protein 2 (GBP2), interferon regulatory factor 5 and 2′-5′-oligoadenylate synthetase 1 (OAS1) genes are involved in three interferon signalling pathways. At present, we do not know whether GBP2 is associated with LN. Therefore, this study focused on the relationship between GBP2 and LN pathogenesis. We speculate that GBP2 may play a role in the pathogenesis of LN as a member of the interferon signalling pathway. Further immunohistochemical results showed that the expression of GBP2 was increased in the renal tissues of LN patients compared with the control group, confirming this conjecture. In conclusion, GBP2 is a member of the interferon signalling pathway that may have implications for the pathogenesis of LN and serves as a potential biomarker for LN. Supplementary Information The online version contains supplementary material available at 10.1186/s12865-022-00520-5.

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“…However, the results were not satisfying, and it was prematurely stopped. Notably, the study on solcitinib pointed out important side effects such as drug reaction with eosinophilia and systemic symptoms (DRESS) and hepatic function modifications, as well as a lack of predicted response [ 74 , 75 , 76 , 77 ].…”

Section: Jak–stat Pathwaymentioning

confidence: 99%

Why Do We Need JAK Inhibitors in Systemic Lupus Erythematosus?

Richter

Cardoneanu

Burlui

et al. 2022

IJMS

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Systemic lupus erythematosus (SLE) is a chronic, multifactorial autoimmune disease with complex pathogenesis characterized by the imbalance of pro-inflammatory and anti-inflammatory cytokines. Janus kinases (JAKs), intracellular non-receptor tyrosine kinases, are essential for signal pathways of many cytokines. The JAK signal transducers and activators of transcription (STAT) pathways consist of four JAK kinases and seven STATs family members. The dysregulation of JAK-STAT pathways represents an important process in the pathogenesis of SLE. Thus, the use of therapies that target specific signaling pathways would be a challenge in SLE. It is well known that JAK inhibitors have real potential for the treatment of rheumatic diseases, but their efficacy in the treatment of SLE remains to be determined. JAK inhibitors are currently being investigated in phase II and III trials and are considered to become the next stage in SLE therapy. In this review, we report the current data regarding the efficacy of JAK inhibitors in SLE. The development of clinically useful kinase inhibitors might improve upon traditional therapeutic strategies.

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A review of advances in the understanding of lupus nephritis pathogenesis as a basis for emerging therapies

Cited by 21 publications

References 133 publications

GBP2 acts as a member of the interferon signaling pathway in lupus nephritis

GBP2 acts as a member of the interferon signaling pathway in lupus nephritis

GBP2 acts as a member of the interferon signalling pathway in lupus nephritis

Why Do We Need JAK Inhibitors in Systemic Lupus Erythematosus?

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