Role of TCF‐1 in differentiation, exhaustion, and memory of CD8
            <sup>+</sup>
            T cells: A review

Zhang, Jiaxue; Lyu, Tong; Cao, Yaming; Feng, Hui

doi:10.1096/fj.202002566r

Cited by 39 publications

(34 citation statements)

References 111 publications

(288 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, CD4 + memory T cells shared an upregulated expression pattern of TFs with CD8 + memory T cells, such as BCLAF1, TCF7, and FOXP1, implying the potential roles of these TFs in regulating the translational initiation in the biological process ( Figure 5H ). Previous studies have indicated that TCF7 and FOXP1 contribute to the development and homeostasis of memory T cells ( 28 , 29 ). CD4 + effector and CD8 + effector T cells also shared some upregulated TFs, including PRDM1, RORA, and KLF6, while CEBPB, CEBPD, CREM, EOMES, and TBX21 were upregulated only in CD8 + effector T cells, which were mainly associated with “regulation of transcription” ( Figure 5I ).…”

Section: Resultsmentioning

confidence: 99%

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction

et al. 2022

View full text Add to dashboard Cite

BackgroundAcute myocardial infarction (AMI) can occur in patients with atherosclerotic disease, with or without plaque rupture. Previous studies have indicated a set of immune responses to plaque rupture. However, the specific circulating immune cell subsets that mediate inflammatory plaque rupture remain elusive.MethodsTen AMI patients were enrolled in our study (five with and five without plaque rupture; plaque characteristics were identified by optical coherence tomography). By single-cell RNA sequencing, we analyzed the transcriptomic profile of peripheral blood mononuclear cells.ResultsWe identified 27 cell clusters among 82,550 cells, including monocytes, T cells, NK cells, B cells, megakaryocytes, and CD34+ cells. Classical and non-classical monocytes constitute the major inflammatory cell types, and pro-inflammatory genes such as CCL5, TLR7, and CX3CR1 were significantly upregulated in patients with plaque rupture, while the neutrophil activation and degranulation genes FPR2, MMP9, and CLEC4D were significantly expressed in the intermediate monocytes derived from patients without plaque rupture. We also found that CD4+ effector T cells may contribute to plaque rupture by producing a range of cytokines and inflammatory-related chemokines, while CD8+ effector T cells express more effector molecules in patients without plaque rupture, such as GZMB, GNLY, and PRF1, which may contribute to the progress of plaque erosion. Additionally, NK and B cells played a significant role in activating inflammatory cells and promoting chemokine production in the plaque rupture. Cell–cell communication elaborated characteristics in signaling pathways dominated by inflammatory activation of classical monocytes in patients with plaque rupture.ConclusionsOur studies demonstrate that the circulating immune cells of patients with plaque rupture exhibit highly pro-inflammatory characteristics, while plaque erosion is mainly associated with intermediate monocyte amplification, neutrophil activation, and degranulation. These findings may provide novel targets for the precise treatment of patients with AMI.

show abstract

Section: Resultsmentioning

confidence: 99%

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction

et al. 2022

View full text Add to dashboard Cite

show abstract

“…TCF7, an active transcription factor associated with the Wnt mediator β-catenin, was induced by basic fibroblast growth factor (bFGF) treatment in fibroblasts (Wang X. et al, 2017). TCF-7 plays an important regulatory role in mature naive CD4 + and CD8 + T cell differentiation, which might participate in the immune response during tissue expansion (Zhang et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Profiling Reveals Important Transcription Factors and Biological Processes in Skin Regeneration Mediated by Mechanical Stretch

Liu

Xiong

et al. 2021

Front. Genet.

View full text Add to dashboard Cite

Background: Mechanical stretch is utilized to promote skin regeneration during tissue expansion for reconstructive surgery. Although mechanical stretch induces characteristic morphological changes in the skin, the biological processes and molecular mechanisms involved in mechanically induced skin regeneration are not well elucidated.Methods: A male rat scalp expansion model was established and the important biological processes related to mechanical stretch-induced skin regeneration were identified using Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and gene set enrichment analysis (GSEA). Analysis was also conducted by constructing a protein–protein interaction (PPI) network, identifying key modules and hub genes, determining transcription factor (TF)-mRNA regulatory relationships, and confirming the expression pattern of the TFs and hub genes.Results: We identified nine robust hub genes (CXCL1, NEB, ACTN3, MYOZ1, ACTA1, TNNT3, PYGM, AMPD1, and CKM) that may serve as key molecules in skin growth. These genes were determined to be involved in several important biological processes, including keratinocyte differentiation, cytoskeleton reorganization, chemokine signaling pathway, glycogen metabolism, and voltage-gated ion channel activity. The potentially significant pathways, including the glucagon signaling pathway, the Wnt signaling pathway, and cytokine–cytokine receptor interaction, were distinguished. In addition, we identified six TFs (LEF1, TCF7, HMGA1, TFAP2C, FOSL1, and ELF5) and constructed regulatory TF–mRNA interaction networks.Conclusion: This study generated a comprehensive overview of the gene networks underlying mechanically induced skin regeneration. The functions of these key genes and the pathways in which they participate may reveal new aspects of skin regeneration under mechanical strain. Furthermore, the identified TF regulators can be used as potential candidates for clinical therapeutics for skin pretreatment before reconstructive surgery.

show abstract

“…Both studies observed that T-cell-targeting escaped epitopes had a diminished expression of the activation marker CD38, intermediate expression of PD-1, which is an activation but also regulatory protein, and a rather high expression of CD127, the receptor of IL-7a that is important for homeostasis [73,74]. Correspondingly, these CD8+ T cells expressed a low level of the transcription factor T-bet and Eomes and a high amount of TCF1, a transcription factor that defines memory-like cells with proliferative potential [112]. This observation is in line with findings in HCV and HIV infection, where the loss of antigen recognition mediated by viral escape led to the formation of a T cell subset that is similar to the memory T cell compartment in acute-resolving infection and that was called memorylike [110,111,113,114].…”

Section: Viral Escapementioning

confidence: 99%

Adaptive Immune Responses, Immune Escape and Immune-Mediated Pathogenesis during HDV Infection

Oberhardt

Hofmann

Thimme

2022

Viruses

View full text Add to dashboard Cite

The hepatitis delta virus (HDV) is the smallest known human virus, yet it causes great harm to patients co-infected with hepatitis B virus (HBV). As a satellite virus of HBV, HDV requires the surface antigen of HBV (HBsAg) for sufficient viral packaging and spread. The special circumstance of co-infection, albeit only one partner depends on the other, raises many virological, immunological, and pathophysiological questions. In the last years, breakthroughs were made in understanding the adaptive immune response, in particular, virus-specific CD4+ and CD8+ T cells, in self-limited versus persistent HBV/HDV co-infection. Indeed, the mechanisms of CD8+ T cell failure in persistent HBV/HDV co-infection include viral escape and T cell exhaustion, and mimic those in other persistent human viral infections, such as hepatitis C virus (HCV), human immunodeficiency virus (HIV), and HBV mono-infection. However, compared to these larger viruses, the small HDV has perfectly adapted to evade recognition by CD8+ T cells restricted by common human leukocyte antigen (HLA) class I alleles. Furthermore, accelerated progression towards liver cirrhosis in persistent HBV/HDV co-infection was attributed to an increased immune-mediated pathology, either caused by innate pathways initiated by the interferon (IFN) system or triggered by misguided and dysfunctional T cells. These new insights into HDV-specific adaptive immunity will be discussed in this review and put into context with known well-described aspects in HBV, HCV, and HIV infections.

show abstract

Role of TCF‐1 in differentiation, exhaustion, and memory of CD8 ⁺ T cells: A review

Cited by 39 publications

References 111 publications

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction

Transcriptome Profiling Reveals Important Transcription Factors and Biological Processes in Skin Regeneration Mediated by Mechanical Stretch

Adaptive Immune Responses, Immune Escape and Immune-Mediated Pathogenesis during HDV Infection

Contact Info

Product

Resources

About

Role of TCF‐1 in differentiation, exhaustion, and memory of CD8 + T cells: A review

Cited by 39 publications

References 111 publications

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction

Single-Cell RNA Sequencing of Peripheral Blood Mononuclear Cells From Acute Myocardial Infarction

Transcriptome Profiling Reveals Important Transcription Factors and Biological Processes in Skin Regeneration Mediated by Mechanical Stretch

Adaptive Immune Responses, Immune Escape and Immune-Mediated Pathogenesis during HDV Infection

Contact Info

Product

Resources

About

Role of TCF‐1 in differentiation, exhaustion, and memory of CD8 ⁺ T cells: A review