ArticleResults in immunology2015
Expression and regulation of Schlafen (SLFN) family members in primary human monocytes, monocyte-derived dendritic cells and T cells.
Article in Results in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 85 citations in OpenAlex.
- Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis.Journal of virology · 2026Review
- SLFN14 functions as a P-TEFb inhibitor to modulate the transcription of HIV-1 and cellular genes.Science advances · 2025Article
- SLFN11, far from being limited to responding to cancer DNA damage.Clinical and experimental medicine · 2025Review
- Surface CD69-Negative CD4 and CD8 Bone Marrow-Resident Human Memory T Cells.European journal of immunology · 2025Article
- The causal effect of natural killer cells on COVID-19 infection, hospitalization and severity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Deciphering the Role of SLFN12: A Novel Biomarker for Predicting Immunotherapy Outcomes in Glioma Patients Through Artificial Intelligence.Journal of cellular and molecular medicine · 2024Article
- Multi-omic signatures of sarcoidosis and progression in bronchoalveolar lavage cells.Respiratory research · 2024Article
- Review
- Schlafens: Emerging Therapeutic Targets.Cancers · 2024Review
- Overview of Structural and Functional Insights of SLFN12 Associated With Different Diseases.Cureus · 2024Review
- Comprehensive analysis of bulk and single-cell RNA sequencing data reveals Schlafen-5 (SLFN5) as a novel prognosis and immunity.International journal of medical sciences · 2024Article
- Research progress of the SLFN family in malignant tumors.Frontiers in oncology · 2024Review
- Integrated analysis of single-cell RNA-seq, bulk RNA-seq, Mendelian randomization, and eQTL reveals T cell-related nomogram model and subtype classification in rheumatoid arthritis.Frontiers in immunology · 2024Article
- Knockdown of Slfn5 alleviates lipopolysaccharide-induced pneumonia by regulating Janus kinase/signal transduction and activator of transcription pathway.Journal of thoracic disease · 2023Article
- Mouse Slfn8 and Slfn9 genes complement human cells lacking SLFN11 during the replication stress response.Communications biology · 2023Article
- Host cell restriction factors of equine infectious anemia virus.Virologica Sinica · 2023Review
- Structural and biochemical characterization of Schlafen11 N-terminal domain.Nucleic acids research · 2023Article
- Schlafen 12 restricts HIV-1 latency reversal by a codon-usage dependent post-transcriptional block in CD4+ T cells.Communications biology · 2023Article
- Velcrin-induced selective cleavage of tRNANature chemical biology · 2023Article
- SLFN5 promotes reversible epithelial and mesenchymal transformation in ovarian cancer.Journal of ovarian research · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Schlafen (SLFN/Slfn) family members have been investigated for their involvement in fundamental cellular processes including growth regulation, differentiation and control of viral replication. However, most research has been focused on the characterization of Slfns within the murine system or in human cell lines. Since little is known about SLFNs in primary human immune cells, we set out to analyze the expression and regulation of the six human SLFN genes in monocytes, monocyte-derived dendritic cells (moDCs) and T cells. Comparison of SLFN gene expression across these three cell types showed high mRNA expression of SLFN11 in monocytes and moDCs and high SLFN5 expression in T cells, indicating functional importance within these cell types. Differentiation of monocytes to moDCs leads to the gradual upregulation of SLFN12L and SLFN13 while SLFN12 levels were decreased by differentiation stimuli. Stimulation of moDCs via human rhinovirus, lipopolysaccharide, or IFN-α lead to strong upregulation of SLFN gene expression, while peptidoglycan poorly stimulated regulation of both SLFNs and the classical interferon-stimulated gene MxA. T cell activation was found to downregulate the expression of SLFN5, SLFN12 and SLFN12L, which was reversible upon addition of exogenous IFN-α. In conclusion, we demonstrate, that SLFN gene upregulation is mainly dependent on autocrine type I interferon signaling in primary human immune cells. Rapid decrease of SLFN expression levels following T cell receptor stimulation indicates a role of SLFNs in the regulation of human T cell quiescence.
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