Multiplex Analysis of Serum Cytokine Profiles in Systemic Lupus Erythematosus and Multiple Sclerosis

Melamud, Mark M.; Ermakov, Evgeny A.; Boiko, Anastasiia S.; Parshukova, D.; Сизиков, А. Э.; Ivanova, Svetlana A.; Baulina, Natalia; Фаворова, О. О.; Nevinsky, Georgy A.; Buneva, Valentina N.

doi:10.3390/ijms232213829

Cited by 21 publications

(11 citation statements)

References 72 publications

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“…This chemokine had been reported to communicate with CCR1, CCR4, and CCR5 receptors on target cells, the expression of CCL3 was elevated in pristine-induced model of SLE. 39 In addition, FISETIN was found to decrease expression of CCL3 and improve the condition of SLE in animal models. 40 CCL3 was also known as an inflammatory marker with differential expression among SLE subjects and other autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

Exploring the role of LIAS-related cuproptosis in systemic lupus erythematosus

Li,

Xu,

Zhang

et al. 2023

Lupus

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Background Cuproptosis is a novel mode of cell death, which is strongly related to energy metabolism in mitochondria and regulated by protein lipoylation. Currently, the molecular mechanisms of cuproptosis-related genes (CRGs) involved in systemic lupus erythematosus (SLE) largely remained unclear, our study is aimed to explore the mechanisms of cuproptosis and CRGs involved in SLE. Methods Bulk RNA-seq datasets were collected to display the expressions of CRGs in peripheral blood mononuclear cells (PBMCs) of SLE and healthy individuals, and then ROC analysis was used to establish the diagnostic models of CRGs. Next, the immune infiltration analyses were applied to reveal the difference of immune cells infiltration in LIAS-low and LIAS-high group. Additionally, WGCNA analysis was performed to find the gene modules significantly correlated with the LIAS expression level. We also performed the functional enrichment analyses for LIAS-related gene modules to determine the potential pathways involved in the development of SLE. Finally, scRNA-seq dataset was used to cluster immune cell subsets, reveal the activated pathways, and study cell-cell interactions in LIAS-low and LIAS-high cells. Result We found CDKN2A was significantly increased and LIAS was significantly decreased in SLE patients compared with healthy individuals. The AUC score showed that LIAS had a great diagnostic value than other CRGs. Additionally, the results of immune infiltration analyses showed that immune cells proportion were diverse in LIAS-low and LIAS-high samples. The gene sets related to LIAS expression level were involved in dephosphorylation of JAK1 by SHP1, phosphorylation of STAT2, cytokine signaling in immune system, expression of interferon-alpha and beta, inhibition of JAK kinase activity by SOCS1/3, and so on. Finally, the results of cell-cell communication showed that CCL- (CCL5 + CCR1) and ANNEXIN- (ANXA1 + FPR1) might play an essential role in the communication network between LIAS-low and LIAS-high cells. Conclusion Above findings inferred that LIAS-mediated cuproptosis might involve in a comprehensive cellular and molecular mechanism to cause the occurrence and development of SLE.

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Section: Discussionmentioning

confidence: 99%

Exploring the role of LIAS-related cuproptosis in systemic lupus erythematosus

Li,

Xu,

Zhang

et al. 2023

Lupus

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“…Some studies have identified increased expression of IL-1β in the serum of SLE patients ( 18 , 19 ) and in lupus-prone mouse models ( 20 ). Our data suggest that IL-1β is not critical for nephritis progression but may in fact have a protective effect that is revealed when its function is inhibited in isolation (as opposed to full inflammasome complex targeting).…”

Section: Discussionmentioning

confidence: 99%

Loss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model

et al. 2023

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Aberrant activation of the innate immune system is a known driver of lupus pathogenesis. Inhibition of the inflammasome and its downstream signaling components in murine models of lupus has been shown to reduce the severity of disease. Interleukin-1 beta (IL-1β) is a proinflammatory cytokine released from cells following inflammasome activation. Here, we examine how loss of IL-1β affects disease severity in the lupus-prone NZM2328 mouse model. We observed a sex-biased increase in immune complex deposition in the kidneys of female mice in the absence of IL-1β that corresponds to worsened proteinuria. Loss of IL-1β did not result in changes in overall survival, anti-dsDNA autoantibody production, or renal immune cell infiltration. RNA-sequencing analysis identified upregulation of TNF and IL-17 signaling pathways specifically in females lacking IL-1β. Increases in these signaling pathways were also found in female patients with lupus nephritis, suggesting clinical relevance for upregulation of these pathways. Together, these data suggest that inhibition of the inflammasome or its downstream elements that block IL-1β signaling may need to be approached with caution in SLE, especially in patients with renal involvement to prevent potential disease exacerbation.

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“…It was reported that CCL3 participated in the in ammatory response by recruiting polymorphonuclear cells. This chemokine had been reported to communicate with CCR1, CCR4 and CCR5 receptors on target cells [46] , the expression of CCL3 was elevated in pristin-induced model of SLE [47] . In addition, FISETIN was found to decrease expression of CCL3 and improve the condition of SLE in animal models [48] .…”

Section: Discussionmentioning

confidence: 99%

Exploring the role of LIAS-related cuproptosis in systemic lupus erythematosus

Zhang

et al. 2023

Preprint

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Background Cuproptosis is a novel mode of cell death, which is strongly related to energy metabolism in mitochondria and regulated by protein lipoylation. Currently, the molecular mechanisms of cuproptosis-related genes (CRGs) involved in systemic lupus erythematosus (SLE) largely remained unclear, our study is aimed to explore the mechanisms of cuproptosis and CRGs involved in SLE. Methods Bulk RNA-seq datasets were collected to display the expressions of CRGs in peripheral blood mononuclear cells (PBMCs) of SLE and healthy individuals, then ROC analysis was used to establish the diagnostic models of CRGs. Next, the immune infiltration analyses were applied to reveal the difference of immune cells infiltration in LIAS-low and LIAS-high group. Additionally, WGCNA analysis was performed to find the gene modules significantly corelated with the LIAS expression level. We also performed the functional enrichment analyses for LIAS-related gene modules to determine the potential pathways involved in the development of SLE. Finally, scRNA-seq dataset was used to cluster immune cell subsets, reveal the activated pathways, and study cell-cell interactions in LIAS-low and LIAS-high cells. Result We found CDKN2A was significantly increased and LIAS was significantly decreased in SLE patients compared with healthy individuals. The AUC score showed that LIAS had a great diagnostic value than other CRGs. Additionally, the results of immune infiltration analyses showed that immune cells proportion were diverse in LIAS-low and LIAS-high samples. The gene sets related to LIAS expression level were involved in dephosphorylation of JAK1 by SHP1, phosphorylation of STAT2, cytokine signaling in immune system, expression of interferon-alpha and beta, inhibition of JAK kinase activity by SOCS1/3 and so on. Finally, the results of cell-cell communication showed that CCL- (CCL5 + CCR1) and ANNEXIN- (ANXA1 + FPR1) might play an essential role in the communication network between LIAS-low and LIAS-high cells. Conclusions Above findings inferred that LIAS-mediated cuproptosis might involve in a comprehensive cellular and molecular mechanism to cause the occurrence and development of SLE.

show abstract

Multiplex Analysis of Serum Cytokine Profiles in Systemic Lupus Erythematosus and Multiple Sclerosis

Cited by 21 publications

References 72 publications

Exploring the role of LIAS-related cuproptosis in systemic lupus erythematosus

Exploring the role of LIAS-related cuproptosis in systemic lupus erythematosus

Loss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model

Exploring the role of LIAS-related cuproptosis in systemic lupus erythematosus

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