IFN-γ, should not be ignored in SLE

Liu, Wenping; Zhang, Shumin; Wang, Jibo

doi:10.3389/fimmu.2022.954706

Cited by 31 publications

(17 citation statements)

References 141 publications

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“…Surprisingly, a higher frequency of IFN-γ + CD4 + T cells was also detected in the mLN of B6mbTrp lo mice ( Figure 1K ). Although there is strong evidence that IFN-γ is pathogenenic in SLE 27 , an anti-inflammatory role has also been reported for this cytokine 28,29 , which may be involved in the FMT experimental setting. Overall, these results suggest that the origin of the microbiota and dietary tryptophan modulate the immune system, with the combination of gut microbiota originating in autoimmune TC mice and high dietary tryptophan promoting autoimmune phenotypes on a non-autoimmune genetic background.…”

Section: Resultsmentioning

confidence: 99%

Dietary tryptophan and genetic susceptibility expand gut microbiota that promote systemic autoimmune activation

Ma,

Ge,

Brown

et al. 2024

Preprint

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Tryptophan modulates disease activity and the composition of microbiota in the B6.Sle1.Sle2.Sle3 (TC) mouse model of lupus. To directly test the effect of tryptophan on the gut microbiome, we transplanted fecal samples from TC and B6 control mice into germ-free or antibiotic-treated non-autoimmune B6 mice that were fed with a high or low tryptophan diet. The recipient mice with TC microbiota and high tryptophan diet had higher levels of immune activation, autoantibody production and intestinal inflammation. A bloom of Ruminococcus gnavus (Rg), a bacterium associated with disease flares in lupus patients, only emerged in the recipients of TC microbiota fed with high tryptophan. Rg depletion in TC mice decreased autoantibody production and increased the frequency of regulatory T cells. Conversely, TC mice colonized with Rg showed higher autoimmune activation. Overall, these results suggest that the interplay of genetic and tryptophan can influence the pathogenesis of lupus through the gut microbiota.

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Section: Resultsmentioning

confidence: 99%

Dietary tryptophan and genetic susceptibility expand gut microbiota that promote systemic autoimmune activation

Ma,

Ge,

Brown

et al. 2024

Preprint

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“…SLE stands as a quintessential autoimmune disorder with the capacity to exert its influence over a myriad of bodily tissues and organs. The hallmark of systemic lupus erythematosus is an exuberant activation of the immune system, culminating in the escalation of autoantibodies and immune complexes, which, in turn, contribute to organ dysfunction [23,24] . Using the currently popular single-cell sequencing technology, we integrated multiple scRNA-seq datasets [25,26] .…”

Section: Discussionmentioning

confidence: 99%

Revealing the Immune Heterogeneity in Systemic Lupus Erythematosus Based on Multi-Omics Data Analysis

Liu,

Gong,

Liu

et al. 2024

Preprint

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Systemic lupus erythematosus is an autoimmune disorder characterized by a spectrum of clinical manifestations. With the progress of next-generation sequencing (NGS) technology, novel techniques for sequencing T cell receptors and B cell receptors have emerged. In this study, we employed the computational approach TRUST4 to construct TCR and BCR libraries using a substantial volume of RNA-seq data extracted from the peripheral blood of sepsis patients. Subsequently, we conducted an analysis to assess the clonality and diversity of the immune repertoire associated with this disease. A total of 30 distinct cell types were annotated and subsequently categorized into 12 clusters. SLE group demonstrated an increase in the innate immune responses of CD14 monocytes, CD16 monocytes, Megakaryocytes, NK cells, and Neutrophis in comparison to the HC group. The CellChat analysis findings unveiled four distinct patterns for input signals and four patterns for output signals. The results of trajectory analysis revealed that the majority of cell subsets are positioned in a single developmental stage. Our research results comprehensively demonstrate the dynamic changes of immune cells during the onset of SLE, and identify specific V and J genes in TCR and BCR that can be used to expand our understanding of SLE.

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“…13 IFN-γ stimulates antigen presentation by monocytes via the JAK-STATs pathway causes chemokine synthesis and is involved in SLE. 14 IFI30 is expressed in the skin and peripheral blood of people with chronic cutaneous lupus erythematosus, and it is markedly elevated in the glomeruli of people with lupus nephritis and systemic lupus erythematosus. 15,16 This gene produces the protein known as RIN2, Ras and Rab interactor 2, which preferentially binds the GTP-bound version of the Rab5 protein and serves as a guanine nucleotide exchange factor for Rab5.…”

Section: Discussionmentioning

confidence: 99%

Identification of monocyte-associated biomarkers in systemic lupus erythematosus and their pan-cancer analysis

Chen,

He,

Wang

et al. 2023

Lupus

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Immune dysregulation is not only a pathogenic mechanism in systemic lupus erythematosus (SLE) but also a potential cause of the link between SLE and cancer. The current understanding of SLE monocyte-associated biomarkers is limited, and the precise mechanism behind the link between SLE and cancer is uncertain. By using WGCNA and immune infiltration to analyze the GSE72326 dataset, we determined the most pertinent modules for monocytes and discovered eight candidate hub genes from them. The limma software was used to find genes that were differently expressed in SLE. The genes that overlapped between the two were chosen using a Venn diagram as the essential genes related to monocytes in SLE, and the essential genes were verified by several datasets. Correlation analysis and GSEA analysis were used to examine the probable immunological pathways connected to key genes. We examined the expression of hub genes in cancer and their interaction with monocytes using the GEPIA and TIMER databases to understand the significance of essential genes in tumorigenesis. In addition, we performed transcription factor identification. We discovered three biomarkers (IFI30, BLVRA, and RIN2) that are mostly involved in interferon-related signaling pathways and are associated with monocyte-mediated immune responses in SLE. The three important genes are also strongly expressed in a number of malignancies and have a relationship with monocytes. As a result, IFI30, BLVRA, and RIN2 may act as SLE-associated biomarkers of monocytes and as a bridge between SLE and tumors. We proposed that interferon-related signaling pathways might function as possible mediators of cancer risk in SLE.

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IFN-γ, should not be ignored in SLE

Cited by 31 publications

References 141 publications

Dietary tryptophan and genetic susceptibility expand gut microbiota that promote systemic autoimmune activation

Dietary tryptophan and genetic susceptibility expand gut microbiota that promote systemic autoimmune activation

Revealing the Immune Heterogeneity in Systemic Lupus Erythematosus Based on Multi-Omics Data Analysis

Identification of monocyte-associated biomarkers in systemic lupus erythematosus and their pan-cancer analysis

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