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pmid:37026011

Identification of key genes and imbalance of immune cell infiltration in immunoglobulin A associated vasculitis nephritis by integrated bioinformatic analysis.

Xianxian Jia · Hua Zhu · Qinglian Jiang · Jia Gu · Shihan Yu · Xuyang Chi · Rui Wang · Yu Shan · Hong Jiang · Xiaoxue Ma

Frontiers in immunology · 2023 doi:10.3389/fimmu.2023.1087293

Paper

complete

Experiment

complete

Data

partial

Analysis

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Execution

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title
Identification of key genes and imbalance of immune cell infiltration in immunoglobulin A associated vasculitis nephritis by integrated bioinformatic analysis.
doi
10.3389/fimmu.2023.1087293
pmid
37026011
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[0]
Xianxian Jia
[1]
Hua Zhu
[2]
Qinglian Jiang
[3]
Jia Gu
[4]
Shihan Yu
[5]
Xuyang Chi
[6]
Rui Wang
[7]
Yu Shan
[8]
Hong Jiang
[9]
Xiaoxue Ma
journal
Frontiers in immunology
year
2023
abstract
Background: IgAV, the most common systemic vasculitis in childhood, is an immunoglobulin A-associated immune complex-mediated disease and its underlying molecular mechanisms are not fully understood. This study attempted to identify differentially expressed genes (DEGs) and find dysregulated immune cell types in IgAV to find the underlying pathogenesis for IgAVN. Methods: GSE102114 datasets were obtained from the Gene Expression Omnibus (GEO) database to identify DEGs. Then, the protein-protein interaction (PPI) network of the DEGs was constructed using the STRING database. And key hub genes were identified by cytoHubba plug-in, performed functional enrichment analyses and followed by verification using PCR based on patient samples. Finally, the abundance of 24 immune cells were detected by Immune Cell Abundance Identifier (ImmuCellAI) to estimate the proportions and dysregulation of immune cell types within IgAVN. Result: A total of 4200 DEGs were screened in IgAVN patients compared to Health Donor, including 2004 upregulated and 2196 downregulated genes. Of the top 10 hub genes from PPI network, STAT1, TLR4, PTEN, UBB, HSPA8, ATP5B, UBA52, and CDC42 were verified significantly upregulated in more patients. Enrichment analyses indicated that hub genes were primarily enriched in Toll-like receptor (TLR) signaling pathway, nucleotide oligomerization domain (NOD)-like receptor signaling pathway, and Th17 signaling pathways. Moreover, we found a diversity of immune cells in IgAVN, consisting mainly of T cells. Finally, this study suggests that the overdifferentiation of Th2 cells, Th17 cells and Tfh cells may be involved in the occurrence and development of IgAVN. Conclusion: We screened out the key genes, pathways and maladjusted immune cells and associated with the pathogenesis of IgAVN. The unique characteristics of IgAV-infiltrating immune cell subsets were confirmed, providing new insights for future molecular targeted therapy and a direction for immunological research on IgAVN.
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A total of 4,200 DEGs were identified in IgAVN samples compared with healthy-donor samples.
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A total of 4,200 DEGs were screened (|Log2fold change| > 2, adjusted p < 0.05) based on the analysis in IgAVN samples compared to HD samples, which contained 2,102 genes with upregulated and 2,098 with downregulated expression.
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Differential expression of long non‑coding RNA and mRNA in children with Henoch‑Schönlein purpura nephritis
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This study attempted to identify differentially expressed genes (DEGs) and find dysregulated immune cell types in IgAV to find the underlying pathogenesis for IgAVN.\nMethods: GSE102114 datasets were obtained from the Gene Expression Omnibus (GEO) database to identify DEGs. Then, the protein-protein interaction (PPI) network of the DEGs was constructed using the STRING database. And key hub genes were identified by cytoHubba plug-in, performed functional enrichment analyses and followed by verification using PCR based on patient samples. Finally, the abundance of 24 immune cells were detected by Immune Cell Abundance Identifier (ImmuCellAI) to estimate the proportions and dysregulation of immune cell types within IgAVN.\nResult: A total of 4200 DEGs were screened in IgAVN patients compared to Health Donor, including 2004 upregulated and 2196 downregulated genes. Of the top 10 hub genes from PPI network, STAT1, TLR4, PTEN, UBB, HSPA8, ATP5B, UBA52, and CDC42 were verified significantly upregulated in more patients. Enrichment analyses indicated that hub genes were primarily enriched in Toll-like receptor (TLR) signaling pathway, nucleotide oligomerization domain (NOD)-like receptor signaling pathway, and Th17 signaling pathways. Moreover, we found a diversity of immune cells in IgAVN, consisting mainly of T cells. Finally, this study suggests that the overdifferentiation of Th2 cells, Th17 cells and Tfh cells may be involved in the occurrence and development of IgAVN.\nConclusion: We screened out the key genes, pathways and maladjusted immune cells and associated with the pathogenesis of IgAVN. 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