T-cell signaling and immunopathologies

Rudd, Christopher E.

doi:10.1007/s00281-010-0203-2

Cited by 3 publications

(2 citation statements)

References 37 publications

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“…SAP and SAP‐related adaptors physically interact with the cytoplasmic tail of SLAM and related receptors to selectively recruit and activate the protein tyrosine kinase Fyn, triggering a signaling cascade that results in receptor phosphorylation and subsequent binding of downstream signaling proteins (28–30). In immune cells, SLAM family receptor activity is important for several critical immunologic functions (19, 21, 31–33).…”

Section: Discussionmentioning

confidence: 99%

Decreased microRNA‐142‐3p/5p expression causes CD4+ T cell activation and B cell hyperstimulation in systemic lupus erythematosus

Ding¹,

Liang²,

Zhao³

et al. 2012

Arthritis & Rheumatism

182

121

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Objective. To examine the role of microRNA-142-3p/5p (miR-142-3p/5p) in the development of autoimmunity in patients with systemic lupus erythematosus (SLE).Methods. MicroRNA-142-3p/5p expression levels were determined by real-time quantitative polymerase chain reaction, and potential target genes were verified using luciferase reporter gene assays. The effects of miR-142-3p/5p on T cell function were assessed by transfection with miR-142-3p/5p inhibitors or mimics. Histone modifications and methylation levels within a putative regulatory region of the miR-142 locus were detected by chromatin immunoprecipitation assay and bisulfite sequencing, respectively.Results. We confirmed that miR-142-3p and miR-142-5p were significantly down-regulated in SLE CD4؉ T cells compared with healthy controls and observed that miR-142-3p/5p levels were inversely correlated with the putative SLE-related targets signaling lymphocytic activation molecule-associated protein (SAP), CD84, and interleukin-10 (IL-10). We demonstrated that miR-142-3p and miR-142-5p directly inhibit SAP, CD84, and IL-10 translation, and that reduced miR-142-3p/5p expression in CD4؉ T cells can significantly increase protein levels of these target genes. Furthermore, inhibiting miR-142-3p/5p in healthy donor CD4؉ T cells caused T cell overactivation and B cell hyperstimulation, whereas overexpression of miR-142-3p/5p in SLE CD4؉ T cells had the opposite effect. We also observed that the decrease in miR-142 expression in SLE CD4؉ T cells correlated with changes to histone modifications and DNA methylation levels upstream of the miR-142 precursor sequence.Conclusion. The results of this study indicate that reduced expression of miR-142-3p/5p in the CD4؉ T cells of patients with SLE causes T cell activity and B cell hyperstimulation.

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Section: Discussionmentioning

confidence: 99%

Decreased microRNA‐142‐3p/5p expression causes CD4+ T cell activation and B cell hyperstimulation in systemic lupus erythematosus

Ding¹,

Liang²,

Zhao³

et al. 2012

Arthritis & Rheumatism

182

121

View full text Add to dashboard Cite

show abstract

“…It is well known that the MAPK signalling pathway and the T-cell receptor signalling pathway are associated with inflammatory responses. 33,34 In addition, activation of the Wnt signalling pathway leads to adverse remodelling after ischaemic injury, whereas inhibition of Wnt signalling improves cardiac function. 35 The ErbB signalling pathway is closely associated with heart failure, and it is a target for drugs to treat heart failure.…”

Section: Discussionmentioning

confidence: 99%

Identification of IL-6 as a potential mediator of the myocardial fibrosis that occurs in response to surgery with cardiopulmonary bypass in children with Tetralogy of Fallot

Liu

Zhang

et al. 2021

Cardiol Young

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Background: Tetralogy of Fallot is a common CHD. Studies have shown a close link between heart failure and myocardial fibrosis. Interleukin-6 has been suggested to be a post-independent factor of heart failure. This study aimed to explore the relationship between IL-6 and myocardial fibrosis during cardiopulmonary bypass. Material and Methods: We downloaded the expression profile dataset GSE132176 from Gene Expression Omnibus. After normalising the raw data, Gene Set Enrichment Analysis and differential gene expression analysis were performed using R. Further, a weighted gene correlation network analysis and a protein–protein interaction network analysis were used to identify HUB genes. Finally, we downloaded single-cell expression data for HUB genes using PanglaoDB. Results: There were 119 differentially expressed genes in right atrium tissues comparing the post-CPB group with the pre-CPB group. IL-6 was found to be significantly up-regulated in the post-CPB group. Six genes (JUN, FOS, ATF3, EGR1, IL-6, and PTGS2) were identified as HUB genes by a weighted gene correlation network analysis and a protein–protein interaction network analysis. Gene Set Enrichment Analysis showed that IL-6 affects the myocardium during CPB mainly through the JAK/STAT signalling pathway. Finally, we used PanglaoDB data to analyse the single-cell expression of the HUB genes. Conclusion: Our findings suggest that high expression of IL-6 and the activation of the JAK/STAT signalling pathway during CPB maybe the potential mechanism of myocardial fibrosis. We speculate that the high expression of IL-6 might be an important factor leading to heart failure after ToF surgery. We expect that these findings will provide a basis for the development of targeted drugs.

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Transcriptomic analysis of reproductive organs of pregnant mice post toxoplasma gondii infection reveals the potential factors that contribute to poor prognosis

Deng,

Chen,

Yang

et al. 2024

Front. Microbiol.

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Toxoplasma gondii is an obligate intracellular parasite of phylum Apicomplexa that poses a huge threat to pregnant hosts, and induces tragic outcomes for pregnant hosts, fetuses and newborns. However, the molecular mechanism underlying the tragic consequences caused by T. gondii remains to be revealed. In the present study, we applied RNA-seq to study the transcriptomic landscape of the whole reproductive organ of pregnant mice post T. gondii infection, aiming to reveal the key altered biological characters of reproductive organs of pregnant mice that could contribute to the tragic outcomes caused by T. gondii infection. The results of the present study showed that the transcriptome of reproductive organs of pregnant mice was significantly altered by T. gondii infection. A total of 2,598 differentially expressed genes (DEGs) were identified, including 1,449 upregulated genes and 1,149 downregulated genes. Enrichment analysis of the DEGs showed that the significantly altered features of reproductive organs of pregnant mice were excessive inflammatory responses, downregulated metabolism processes, and congenital diseases. The chemotaxis of immune cells in the reproductive organs of infected pregnant mice could also be reshaped by 19 differentially expressed chemokines and 6 differentially expressed chemokine receptors that could contribute to the damages of reproductive organ in pregnant mice. Overall, the findings of present study may help to understand the pathogenic mechanism of the acute T. gondii infection in reproductive organs of pregnant mice, and it could also help to improve toxoplasmosis therapeutics for pregnant individuals.

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T-cell signaling and immunopathologies

Cited by 3 publications

References 37 publications

Decreased microRNA‐142‐3p/5p expression causes CD4+ T cell activation and B cell hyperstimulation in systemic lupus erythematosus

Decreased microRNA‐142‐3p/5p expression causes CD4+ T cell activation and B cell hyperstimulation in systemic lupus erythematosus

Identification of IL-6 as a potential mediator of the myocardial fibrosis that occurs in response to surgery with cardiopulmonary bypass in children with Tetralogy of Fallot

Transcriptomic analysis of reproductive organs of pregnant mice post toxoplasma gondii infection reveals the potential factors that contribute to poor prognosis

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