Ask about this productRelated genes to: IFI44L Blocking Peptide
- Gene:
- IFI44L NIH gene
- Name:
- interferon induced protein 44 like
- Previous symbol:
- C1orf29
- Synonyms:
- GS3686
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-29
- Date modifiied:
- 2016-10-05
Related products to: IFI44L Blocking Peptide
Related articles to: IFI44L Blocking Peptide
- Chemoradiotherapy (CRT) represents a cornerstone treatment for colorectal cancer (CRC), yet heterogeneous responses to CRT in treatment response remain a major clinical challenge. Increasing evidence suggests that the tumor immune microenvironment (TME) especially intratumoral CD8 T cells plays an important role in determining CRT efficacy; however, the molecular mechanisms linking tumor-derived factors to immune-mediated treatment sensitivity remain poorly understood. Here, we aimed to identify and characterize regulators of CRT response and the underline mechanisms in CRC. - Source: PubMed
Publication date: 2026/08/28
Zheng LinlinLi MengjieYan RuoqingTan Wen - Vaccination (immune priming) against Ostreid herpesvirus 1 (OsHV-1) is a strategy for managing Pacific Oyster Mortality Syndrome (POMS), yet the transcriptional mechanisms underlying protection remain poorly defined. We evaluated the transcriptome in Pacific oysters (Magallana gigas) administered heat-treated (HT) and live OsHV-1 vaccines at 18 °C and 22 °C. All priming strategies improved survival after challenge with virulent OsHV-1 at 22 °C, with relative percent survival of 57.5% for HT OsHV-1 administered at 18 °C, 76.2% for HT OsHV-1 at 22 °C and 85.0% for live OsHV-1 at 18 °C. Primed surviving oysters exhibited significantly lower viral loads after challenge than controls, with distinct transcriptomic responses among live and HT OsHV-1 treatments. Live OsHV-1, which provided the highest protection, triggered a rapid antiviral response one day after priming, characterised by upregulation of predicted orthologs of viral RNA sensors and interferon-stimulated-like signalling components including RLR-family genes, DHX58, IFI44L and a MAVS-like adaptor. In contrast, HT OsHV-1 induced a delayed response on day four, enriched for protein quality control, endoplasmic reticulum-associated degradation and ribosome biogenesis pathways. By day 12, gene expression of primed oysters had returned to baseline. In live OsHV-1-primed oysters, post-challenge gene modules were enriched for predicted orthologs of antiviral and immune signalling components and DNA replication regulators, indicative of a coordinated antiviral response and increased haemocyte activity. Overall, these results highlight transcriptional signatures underlying OsHV-1-based vaccination, which is developing as a strategy in integrated POMS management. - Source: PubMed
Publication date: 2026/09/10
Hossain ArmanWhittington RichardCosta Vincenzo ACampbell Lee KPathirana ErandiSamsing Francisca - BackgroundSystemic Lupus Erythematosus (SLE) is a heterogeneous autoimmune disease characterized by dysregulated type I interferon signaling. Epigenetic alterations, particularly DNA methylation changes in interferon-regulated genes, have emerged as promising biomarkers for disease diagnosis and stratification. Among these, IFI44L promoter hypomethylation has been repeatedly reported as one of the most consistent and disease specific in SLE.ObjectiveTo systematically evaluate the evidence on IFI44L promoter methylation in SLE and to quantitatively synthesize its epigenetic and diagnostic performance across diverse populations using meta-analytic approaches.MethodsA systematic search of published literature was conducted to identify studies reporting IFI44L promoter methylation in patients with SLE and controls. Study characteristics, ethnicity, cell type, direction of methylation, CpG hypo/hyper methylation counts were extracted. Descriptive analyses were performed across ethnicities and cell types. Diagnostic performance was summarized as the pooled area under the receiver operating characteristic (ROC) curve (AUC). Variance of AUC estimates was approximated using the Hanley-McNeil method, and a random-effects meta-analysis (DerSimonian-Laird) was applied to account for between-study heterogeneity.Results16 study datasets reporting hypomethylation of the IFI44L promoter were included. IFI44L promoter hypomethylation was consistently observed across ethnic groups and biological sample types. Descriptive subgroup analyses identified heterogeneity in the magnitude of IFI44L promoter hypomethylation across ethnic groups, study periods, and methylation profiling methodologies, whereas differences according to biological sample type were less pronounced and did not reach statistical significance. Hypomethylation predominated over hypermethylation among studies reporting both methylation directions. Diagnostic AUC values varied across studies but were largely independent of sample size and the magnitude of hypomethylation. The pooled area under the curve (AUC) was 0.74 (95% CI 0.64-0.84), indicating moderate overall diagnostic performance.ConclusionIFI44L promoter hypomethylation represents a significant and reproducible epigenetic signature of SLE across populations and study designs. Despite variability in methylation magnitude, its diagnostic performance remains consistent, supporting IFI44L methylation as a promising biomarker for SLE. - Source: PubMed
Publication date: 2026/08/20
Sheraz KainatFagbo AasiyahSiddique RahemeenAlhodathi LeenSheraz WahidullahUsman Muhammad AhmedMushtaq Mazhar - Behçet's disease (BD) is a rare chronic systemic vasculitis of unknown etiology. The heterogeneity of peripheral blood immune cells and the dysregulation of intercellular communication in BD remain insufficiently characterized. The present study employs single-cell transcriptomics to comprehensively delineate the peripheral blood immune cell atlas of BD, identify candidate diagnostic biomarkers, and dissect the remodeling patterns of intercellular communication networks. - Source: PubMed
Publication date: 2026/08/04
Yang YanfeiChen Yuexin - Human Immunodeficiency Virus (HIV) infection impairs the immune system, diminishing its ability to defend against pathogens and increasing susceptibility to infections and diseases. To gain a comprehensive understanding of the heterogeneity, functions, and regulatory mechanisms of immune cells affected by different HIV viral loads, we investigated the biological impacts of HIV infection on the human body. We reanalyzed a publicly available peripheral blood mononuclear cell (PBMC) single-cell RNA sequencing dataset (GSE157829) comprising three people living with HIV with high viral load (HL-HIV), three people living with HIV with low viral load (LL-HIV), and one healthy control donor. We constructed single-cell immune atlases that represent different viral load profiles. We also analyzed the dynamic changes in specific immune cell subpopulations to gain insights into their signaling pathways, developmental trajectories, and key transcriptional regulators. At the single-cell level, non-classical monocyte subpopulations, specifically ncMono_LYN_TCF7L2 and ncMono_IL32, functioned as immunosurveillance elements but also activated pro-inflammatory pathways, leading to immune activation. B_CD83 subpopulation was critical in B cell development, facilitating B cell differentiation and tolerance. Naive.T_TNFAIP3 subpopulation exhibited anti-inflammatory effects and protected against aberrant apoptosis. Central memory T (TCM)_TCF7_CCR7 subpopulation played a crucial role in regulating the expansion of HIV-specific CD8 T cells and maintaining the immune response. Additionally, we observed a significant enrichment of IFI44L-positive subpopulations across different cell types, particularly in HL-HIV samples. Our findings demonstrate that HIV infection increases the complexity of immune cell subpopulations. Notably, IFI44L has emerged as a potential disease hub gene in HL-HIV samples, highlighting its potential as a novel biomarker for HIV. - Source: PubMed
Publication date: 2026/08/17
Gao JiaminLi YanjunHuang JinpingHuang XianzhenZhu QingdongWei CailingChen JielingLuo ShundaXie Zhouhua