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Journal articles on the topic 'ISGs phenotype'

Author: Grafiati

Published: 11 March 2023

Last updated: 31 July 2025

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1

Swieboda, Dominika, Erica Johnson, Ioanna Skountzou, and Rana Chakraborty. "Baby’s First Macrophage: How do placental macrophages (Hofbauer Cells, HCs) contribute to immune tolerance and infection response during pregnancy?" Journal of Immunology 202, no. 1_Supplement (2019): 126.28. http://dx.doi.org/10.4049/jimmunol.202.supp.126.28.

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Abstract Placental immunity is dichotomous: tolerance of the semiallogenic fetus is balanced with limiting transmission of maternal pathogens. HCs are the major fetal immune cell at the placenta, but mechanisms responsible for maintaining immune homeostasis while preventing infection require elucidation. We determined the phenotype of human HCs throughout gestation and analyzed stimulation response. Activated HCs were present in early pregnancy and reduced in number by term while maintaining similar phenotypes. Tolerant HC numbers were highest in midgestation, after a relatively intolerant phe

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Morrison, Robert J., Nicolas-George Katsantonis, Kevin M. Motz, et al. "Pathologic Fibroblasts in Idiopathic Subglottic Stenosis Amplify Local Inflammatory Signals." Otolaryngology–Head and Neck Surgery 160, no. 1 (2018): 107–15. http://dx.doi.org/10.1177/0194599818803584.

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Objective To characterize the phenotype and function of fibroblasts derived from airway scar in idiopathic subglottic stenosis (iSGS) and to explore scar fibroblast response to interleukin 17A (IL-17A). Study Design Basic science. Setting Laboratory. Subjects and Methods Primary fibroblast cell lines from iSGS subjects, idiopathic pulmonary fibrosis subjects, and normal control airways were utilized for analysis. Protein, molecular, and flow cytometric techniques were applied in vitro to assess the phenotype and functional response of disease fibroblasts to IL-17A. Results Mechanistically, IL-

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Gluchowski, Marcel, Xiaoqiong Yu, Bernard Abrenica, et al. "Transient Increases in Inflammation and Proapoptotic Potential Are Associated with the HESN Phenotype Observed in a Subgroup of Kenyan Female Sex Workers." Viruses 14, no. 3 (2022): 471. http://dx.doi.org/10.3390/v14030471.

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Interferon (IFN) -stimulated genes (ISGs) are critical effectors of IFN response to viral infection, but whether ISG expression is a correlate of protection against HIV infection remains elusive. A well-characterized subcohort of Kenyan female sex workers, who, despite being repeatedly exposed to HIV-1 remain seronegative (HESN), exhibit reduced baseline systemic and mucosal immune activation. This study tested the hypothesis that regulation of ISGs in the cells of HESN potentiates a robust antiviral response against HIV. Transcriptional profile of a panel of ISGs with antiviral function in PB

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Gupta, Sarthak, Shuichiro Nakabo, Luz P. Blanco, et al. "Sex differences in neutrophil biology modulate response to type I interferons and immunometabolism." Proceedings of the National Academy of Sciences 117, no. 28 (2020): 16481–91. http://dx.doi.org/10.1073/pnas.2003603117.

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Differences between female and male immunity may contribute to variations in response to infections and predisposition to autoimmunity. We previously reported that neutrophils from reproductive-age males are more immature and less activated than their female counterparts. To further characterize the mechanisms that drive differential neutrophil phenotypes, we performed RNA sequencing on circulating neutrophils from healthy adult females and males. Female neutrophils displayed significant up-regulation of type I IFN (IFN)-stimulated genes (ISGs). Single-cell RNA-sequencing analysis indicated th

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Hancock, Meaghan H., Karen L. Mossman, and James R. Smiley. "Cell Fusion-Induced Activation of Interferon-Stimulated Genes Is Not Required for Restriction of a Herpes Simplex Virus VP16/ICP0 Mutant in Heterokarya Formed between Permissive and Restrictive Cells." Journal of Virology 83, no. 17 (2009): 8976–79. http://dx.doi.org/10.1128/jvi.00142-09.

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ABSTRACT Herpes simplex virus VP16 and ICP0 mutants replicate efficiently in U2OS osteosarcoma cells but are restricted in other cell types. We previously showed that the restrictive phenotype is dominant in a transient cell fusion assay, suggesting that U2OS cells lack an antiviral mechanism present in other cells. Recent data indicate that unscheduled membrane fusion events can activate the expression of interferon-stimulated genes (ISGs) in fibroblasts, raising the possibility that our earlier results were due to a fusion-induced antiviral state. However, we show here that the permissive ph

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Jurczyszak, Denise, Lara Manganaro, Sofija Buta, et al. "ISG15 deficiency restricts HIV-1 infection." PLOS Pathogens 18, no. 3 (2022): e1010405. http://dx.doi.org/10.1371/journal.ppat.1010405.

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Type I interferons (IFN-Is) are a group of potent inflammatory and antiviral cytokines. They induce IFN stimulated genes (ISGs), which act as proinflammatory mediators, antiviral effectors, and negative regulators of the IFN-I signaling cascade itself. One such regulator is interferon stimulated gene 15 (ISG15). Humans with complete ISG15 deficiency express persistently elevated levels of ISGs, and consequently, exhibit broad spectrum resistance to viral infection. Here, we demonstrate that IFN-I primed fibroblasts derived from ISG15-deficient individuals are more resistant to infection with s

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Chan, Jennie, Peter Liehl, Rosane DeOliveira, et al. "Dual role of type I IFN during plasmodium infection (P3056)." Journal of Immunology 190, no. 1_Supplement (2013): 125.6. http://dx.doi.org/10.4049/jimmunol.190.supp.125.6.

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Abstract The molecular mechanisms regulating the inflammatory response during malaria are still poorly defined. Inflammatory cytokines and type I IFNs induced when innate immune sensors recognize components of the malaria parasite can contribute to clearance of the parasite and in some circumstances these same effectors lead to experimental cerebral malaria (ECM). Infection of C57BL/6 mice with Plasmodium berghei ANKA (PbA) leads to ECM where animals succumb to infection and die. Upon infection with PbA infected red blood cells (iRBCs), C57/Bl6 mice succumb to death 6-12 days post-infection. R

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Thomas, Emmanuel, Mazen Noureddin, Yaron Rotman, and T. Jake Liang. "Mechanism of induction and genotype-phenotype correlation of IL28B and ISG expression in HCV-infected primary human hepatocytes and liver (P1383)." Journal of Immunology 190, no. 1_Supplement (2013): 57.3. http://dx.doi.org/10.4049/jimmunol.190.supp.57.3.

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Abstract Background: IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs. However, the intrinsic innate immune response following HCV infection remains poorly understood. Methods: Immunofluorescence staining of innate immune molecules (IRF3, ISG15) were performed on HCV infected PHHs. PHHs were also studied for correlation of IL28 genotype with type III IFN and ISG expression. In addition, RNA was extracted from 60 pre-treatment archived liver biopsies and hepatic expression of IFNs was measured by qPCR. Rs12979860 genotype

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Foxman, Ellen F., James A. Storer, Megan E. Fitzgerald, et al. "Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells." Proceedings of the National Academy of Sciences 112, no. 3 (2015): 827–32. http://dx.doi.org/10.1073/pnas.1411030112.

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Most isolates of human rhinovirus, the common cold virus, replicate more robustly at the cool temperatures found in the nasal cavity (33–35 °C) than at core body temperature (37 °C). To gain insight into the mechanism of temperature-dependent growth, we compared the transcriptional response of primary mouse airway epithelial cells infected with rhinovirus at 33 °C vs. 37 °C. Mouse airway cells infected with mouse-adapted rhinovirus 1B exhibited a striking enrichment in expression of antiviral defense response genes at 37 °C relative to 33 °C, which correlated with significantly higher expressi

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Ganguly, Payal, Agata Burska, Charlotte Davis, Jehan J. El-Jawhari, Peter V. Giannoudis та Elena Jones. "Intrinsic Type 1 Interferon (IFN1) Profile of Uncultured Human Bone Marrow CD45lowCD271+ Multipotential Stromal Cells (BM-MSCs): The Impact of Donor Age, Culture Expansion and IFNα and IFNβ Stimulation". Biomedicines 8, № 7 (2020): 214. http://dx.doi.org/10.3390/biomedicines8070214.

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Skeletal aging is associated with reduced proliferative potential of bone marrow (BM) multipotential stromal cells (MSCs). Recent data suggest the involvement of type 1 interferon (IFN1) signalling in hematopoietic stem cell (HSC) senescence. Considering that BM-HSCs and BM-MSCs share the same BM niche, we investigated IFN1 expression profile in human BM-MSCs in relation to donor age, culture-expansion and IFN1 (α and β) stimulation. Fluorescence-activated cell sorting was used to purify uncultured BM-MSCs from younger (19–41, n = 6) and older (59–89, n = 6) donors based on the CD45lowCD271+ p

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Dorrington, Michael G., Sinu John, and Iain D. C. Fraser. "Type I IFN mediates cell-intrinsic host protective effects during acute gram-negative bacterial infection of macrophages." Journal of Immunology 198, no. 1_Supplement (2017): 123.7. http://dx.doi.org/10.4049/jimmunol.198.supp.123.7.

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Abstract Many bacteria require entrance into host immune cells, such as macrophages, in order to replicate. These intracellular bacteria have evolved complex strategies for avoiding the antimicrobial programming of these immune cells to create replicative niches. While we know a great deal about various virulence factors deployed by intracellular bacteria as well as how cells try to kill these pathogens, how bacteria and host cells modulate each others’ responses during infection is less well understood. Using the Gram-negative bacteria Burkholderia cenocepacia, we have uncovered a negative re

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Mar, Katrina Bockying, Jennifer Eitson, and John Schoggins. "Interferon-stimulated gene LY6E enhances entry of diverse RNA viruses." Journal of Immunology 196, no. 1_Supplement (2016): 217.7. http://dx.doi.org/10.4049/jimmunol.196.supp.217.7.

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Abstract The type I interferon (IFN) response is the primary cellular defense mechanism against viruses. IFN protects against viral infection by activating the expression of hundreds of interferon-stimulated genes (ISGs), some of which have potent antiviral effector activity. Our recent screening efforts to identify novel antiviral ISGs unexpectedly uncovered a small subset of genes that enhanced viral infectivity. The goals of this project are to characterize the mechanism of LY6E, an ISG that enhanced unrelated viruses from multiple families. Here we show that ectopic expression of LY6E enha

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Lucas, Tiffany M., Justin M. Richner, and Michael S. Diamond. "The Interferon-Stimulated GeneIfi27l2aRestricts West Nile Virus Infection and Pathogenesis in a Cell-Type- and Region-Specific Manner." Journal of Virology 90, no. 5 (2015): 2600–2615. http://dx.doi.org/10.1128/jvi.02463-15.

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ABSTRACTThe mammalian host responds to viral infections by inducing expression of hundreds of interferon-stimulated genes (ISGs). While the functional significance of many ISGs has yet to be determined, their cell type and temporal nature of expression suggest unique activities against specific pathogens. Using a combination of ectopic expression and gene silencing approaches in cell culture, we previously identifiedIfi27l2aas a candidate antiviral ISG within neuronal subsets of the central nervous system (CNS) that restricts infection by West Nile virus (WNV), an encephalitic flavivirus of gl

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Garau, Jessica, Vanessa Cavallera, Marialuisa Valente, et al. "Molecular Genetics and Interferon Signature in the Italian Aicardi Goutières Syndrome Cohort: Report of 12 New Cases and Literature Review." Journal of Clinical Medicine 8, no. 5 (2019): 750. http://dx.doi.org/10.3390/jcm8050750.

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Aicardi-Goutières syndrome (AGS) is a genetically determined early onset encephalopathy characterized by cerebral calcification, leukodystrophy, and increased expression of interferon-stimulated genes (ISGs). Up to now, seven genes (TREX1, RNASEH2B, RNASEH2C, RNASEH2A, ADAR1, SAMHD1, IFIH1) have been associated with an AGS phenotype. Next Generation Sequencing (NGS) analysis was performed on 51 AGS patients and interferon signature (IS) was investigated in 18 AGS patients and 31 healthy controls. NGS identified mutations in 48 of 51 subjects, with three patients demonstrating a typical AGS phe

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von Recum-Knepper, Jessica, Anne Sadewasser, Viola K. Weinheimer, and Thorsten Wolff. "Fluorescence-Activated Cell Sorting-Based Analysis Reveals an Asymmetric Induction of Interferon-Stimulated Genes in Response to Seasonal Influenza A Virus." Journal of Virology 89, no. 14 (2015): 6982–93. http://dx.doi.org/10.1128/jvi.00857-15.

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ABSTRACTInfluenza A virus (IAV) infection provokes an antiviral response involving the expression of type I and III interferons (IFN) and IFN-stimulated genes (ISGs) in infected cell cultures. However, the spatiotemporal dynamics of the IFN reaction are incompletely understood, as previous studies investigated mainly the population responses of virus-infected cultures, although substantial cell-to-cell variability has been documented. We devised a fluorescence-activated cell sorting-based assay to simultaneously quantify expression of viral antigens and ISGs, such as ISG15, MxA, and IFIT1, in

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Kanashiro, Maria Alejandra, Sudip Kumar Paul, Masamitsu Sone, et al. "iPSC-Derived Mesenchymal Stem Cells Supports the Ex Vivo expansion of Human Hematopoietic Stem and Progenitor Cells Via Sterile Inflammation Pathway." Blood 142, Supplement 1 (2023): 2680. http://dx.doi.org/10.1182/blood-2023-181378.

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Ex-vivo expansion of human hematopoietic stem/progenitor cells (HSPCs) represents a promising technology for investigating HSPCs' function and overcoming donor shortage for transplantation. HSPCs appropriately regulate self-renewal and differentiation, relying on hematopoietic supporting cells within the bone marrow microenvironment. Notably, various strategies employing primary mesenchymal stem cells (MSCs) as hematopoietic supporting cells have demonstrated successful HSPC expansion (De Lima, et al, N. Engl. J. Med. 2012). However, the preparation of primary MSCs includes harmful procedures,

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Wagner, Allison, Chi Weindel, Robert Watson, and Kristin Patrick. "Alternative splicing of Bax controls cell death and innate immune responses in macrophages." Journal of Immunology 206, no. 1_Supplement (2021): 97.01. http://dx.doi.org/10.4049/jimmunol.206.supp.97.01.

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Abstract To defend against invading pathogens, the macrophage innate immune response requires rapid, robust gene expression reprogramming. Innate immune genes that are induced as part of this response are regulated at many steps. While transcriptional activation of innate immune genes has been extensively studied, the mechanisms driving their post-transcriptional regulation (i.e. alternative splicing) needs further investigation. To begin learning how pre-mRNA splicing changes impact the innate immune response in macrophages, we examined how loss of a splicing regulatory protein called SRSF6 (

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Duong, Francois H. T., Gaia Trincucci, Tujana Boldanova та ін. "IFN-λ receptor 1 expression is induced in chronic hepatitis C and correlates with the IFN-λ3 genotype and with nonresponsiveness to IFN-α therapies". Journal of Experimental Medicine 211, № 5 (2014): 857–68. http://dx.doi.org/10.1084/jem.20131557.

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The molecular mechanisms that link IFN-λ3 genotypes to differential induction of interferon (IFN)-stimulated genes (ISGs) in the liver of patients with chronic hepatitis C (CHC) are not known. We measured the expression of IFN-λ and of the specific IFN-λ receptor chain (IFN-λR1) in 122 liver biopsies of patients with CHC and 53 control samples. The IFN-λ3 genotype was not associated with differential expression of IFN-λ, but rather IFN-λR1. In a series of 30 primary human hepatocyte (PHH) samples, IFN-λR1 expression was low but could be induced with IFN-α. IFN-α–induced IFN-λR1 expression was

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Paul, Kausik, June Young Lee, Rosario Hernandez-Armengol, Tomohiro Shibata, Caroline Anne Jefferies, and David R. Gibb. "Type 1 interferons promote anti-RBC antibody responses in interferon-dependent lupus mice." Journal of Immunology 210, no. 1_Supplement (2023): 247.12. http://dx.doi.org/10.4049/jimmunol.210.supp.247.12.

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Abstract Red blood cell (RBC) transfusion can induce anti-RBC antibodies that promote hemolytic events. Patients with systemic lupus erythematosus (SLE) have an increased frequency of RBC alloimmunization, and two-thirds of patients express a type 1 interferon (IFNα/β) gene signature. We previously reported that IFNα/β induces RBC alloimmunization in the IFNα/β-dependent pristane lupus mouse model. However, it is unclear whether the lupus-like phenotype or IFNα/β directly promoted alloimmunization. Thus, we examined alloantibody responses in MRL/lpr mice, which have an IFNα/β-independent lupus

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Marker, Rebecca, Aidan Moriarty, Remi Klotz, and Min Yu. "Abstract 903: Mechanisms mediating hypoxic memory of type I IFN signaling suppression and implications for immune evasion in luminal breast cancer cells." Cancer Research 85, no. 8_Supplement_1 (2025): 903. https://doi.org/10.1158/1538-7445.am2025-903.

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Abstract Solid tumors often contain patches of hypoxic regions that yield aggressive, pro-metastatic phenotypes. Prevention and understanding of metastases is critical for the future of breast cancer research, as metastatic cancer is extremely difficult to manage and treat. Recent work in our lab has shown that long-term hypoxia suppresses type I interferon (IFN) signaling in breast cancer cells. Even upon reoxygenation, these gene expression changes are maintained, indicative of “hypoxic memory.” Breast cancer cells that have disseminated from the primary tumor as circulating tumor cells with

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Wang, Qingde, Xiaoni Li, Ruofan Qi, Wenshuo Zhang, Pengyuan Zheng, and Timothy R. Billiar. "RNA editing is required for innate immune homeostasis through inhibiting cytosolic RNA receptor MDA-5 activated by cellular endogenous RNAs." Journal of Immunology 200, no. 1_Supplement (2018): 169.3. http://dx.doi.org/10.4049/jimmunol.200.supp.169.3.

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Abstract Cytosolic RNA receptors, RLRs, play an essential role in antiviral infections that specifically detect the invaded viral RNAs leading to IFN and ISG expression and antiviral reactions through RNA sensing signaling pathways. This viral RNA sensing mechanism tolerate cellular “self” RNA in normal cells. However, how RLRs distinguish viral and self RNA molecules remains ambiguous. Our recent study showed that insufficient RNA editing by editing enzyme ADAR1 enables the cellular endogenous RNAs to stimulate the RLRs and activate the innate immune signaling pathway that lead to type I IFN

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Scott, Haley M., Allison R. Wagner, Kelsi West, Robert Watson, and Kristin L. Patrick. "Serine Arginine Splicing Factor 7 (SRSF7) is a critical regulator of innate immune activation in macrophages." Journal of Immunology 208, no. 1_Supplement (2022): 163.29. http://dx.doi.org/10.4049/jimmunol.208.supp.163.29.

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Abstract Macrophages are immune cells that receive signals from pathogens and respond by reprogramming gene expression to activate an innate immune response. We currently have a poor understanding of how this response is fine-tuned at a post-transcriptional level. To address this, we turned to recent proteomics studies that identified mRNA processing as a pathway enriched for differentially phosphorylated proteins in macrophages infected with the important human pathogen Mycobacterium tuberculosis (Mtb). We became interested in one of these mRNA processing proteins, a splicing regulatory facto

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Talukdar, Priyanka, Joshua T. Mattila, and Beth A. Fallert Junecko. "Type III interferons are expressed in tuberculosis granulomas and promote an inflammatory phenotype in macrophages that differs from type I interferon." Journal of Immunology 204, no. 1_Supplement (2020): 149.15. http://dx.doi.org/10.4049/jimmunol.204.supp.149.15.

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Abstract Humans and non-human primates express four subtypes of type III interferons (IFNλs; IFNλ1-IFNλ4). Unlike type I interferons, which have been thoroughly investigated in tuberculosis (TB), the role of IFNλs and their effects on immunity in TB remain unknown, especially at the disease site. To better understand the role of IFNλs in TB, we examined IFNλ1 and IFNλ4 expression in cynomolgus macaques with TB and investigated the effects of IFNα/β, IFNλ1 and IFNλ4 signaling on macaque macrophages. Using IHC, we identified differential IFNλ1 and IFNλ4 expression in macrophages and neutrophils,

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Li, Jian, Josephine Mun-Yee Ko, Wei Dai, et al. "Depletion of DNA Polymerase Theta Inhibits Tumor Growth and Promotes Genome Instability through the cGAS-STING-ISG Pathway in Esophageal Squamous Cell Carcinoma." Cancers 13, no. 13 (2021): 3204. http://dx.doi.org/10.3390/cancers13133204.

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Overexpression of the specialized DNA polymerase theta (POLQ) is frequent in breast, colon and lung cancers and has been correlated with unfavorable clinical outcomes. Here, we aimed to determine the importance and functional role of POLQ in esophageal squamous cell carcinoma (ESCC). Integrated analysis of four RNA-seq datasets showed POLQ was predominantly upregulated in ESCC tumors. High expression of POLQ was also observed in a cohort of 25 Hong Kong ESCC patients and negatively correlated with ESCC patient survival. POLQ knockout (KO) ESCC cells were sensitized to multiple genotoxic agents

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Farina, Giuseppina Alessandra, Antonella Farina, Mara Cirone, et al. "Epstein-Barr virus infection induces aberrant TLR/MyD88 activation pathway and fibroblast-myofibroblast conversion in systemic sclerosis. (P6322)." Journal of Immunology 190, no. 1_Supplement (2013): 182.13. http://dx.doi.org/10.4049/jimmunol.190.supp.182.13.

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Abstract Activated fibroblasts, mainly myofibroblasts are considered the principal mediators of fibrogenesis in systemic sclerosis (SSc), although the origin of persistent activation of fibroblasts and myofibroblasts is unclear. Activation of Interferon by Toll-like receptors in immune cells may play a role in the pathogenesis of inflammation in many autoimmune diseases, including SSc. We investigated whether fibroblasts persistently activated by innate immune and infectious stimuli might induce IFNs and TGFβ, two major markers of inflammation and fibrosis implicated in SSc pathogenesis. Since

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Hirayama, T., H. Konaka, Y. Kato, H. Takamatsu, and A. Kumanogoh. "AB0143 VORINOSTAT IMPROVES THE PATHOGENESIS OF SLE MODEL MICE BY SUPPRESSING IFN-I AND TLR7/8 SIGNALS." Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 1251.1–1251. http://dx.doi.org/10.1136/annrheumdis-2023-eular.2874.

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BackgroundSLE is a systemic autoimmune disease caused by impaired innate and acquired immune tolerance, resulting in increased Type I IFN (IFN-I) and aberrant B cell development, in which cGAS and TLR 7/8 signaling play critical roles.TLR7/8 and cGAS signal is activated due to the overresponse to nucleic acid derived from impaired clearance of apoptotic cells, which leads to increased IFN-I production. Activation of TLR7/8 signaling also leads to the development of abnormal B cell populations, including short-lived plasma blasts, double negative B cells (DNB), and active native B (NAB). It sug

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Kim, Min-Jung, Sun-Young Hwang, Tadaatsu Imaizumi, and Joo-Yeon Yoo. "Negative Feedback Regulation of RIG-I-Mediated Antiviral Signaling by Interferon-Induced ISG15 Conjugation." Journal of Virology 82, no. 3 (2007): 1474–83. http://dx.doi.org/10.1128/jvi.01650-07.

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ABSTRACT RIG-I senses intracellular virus-specific nucleic acid structures and initiates an antiviral response that induces interferon (IFN) production, which, in turn, activates the transcription of RIG-I to increase RIG-I protein levels. Upon intracellular poly(I:C) stimulation, however, the levels of RIG-I protein did not correlate with the expression patterns of RIG-I transcripts. When the ISG15 conjugation system was overexpressed, ISG15 was conjugated to RIG-I and cellular levels of the unconjugated form of RIG-I decreased. The ISGylation of RIG-I reduced levels of both basal and virus-i

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Dai, Manman, Shibing Li, Keyi Shi, Jiayu Liao, Hui Sun, and Ming Liao. "Systematic Identification of Host Immune Key Factors Influencing Viral Infection in PBL of ALV-J Infected SPF Chicken." Viruses 12, no. 1 (2020): 114. http://dx.doi.org/10.3390/v12010114.

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Although research related to avian leukosis virus subgroup J (ALV-J) has lasted for more than a century, the systematic identification of host immune key factors against ALV-J infection has not been reported. In this study, we establish an infection model in which four-week-old SPF chickens are infected with ALV-J strain CHN06, after which the host immune response is detected. We found that the expression of two antiviral interferon-stimulated genes (ISGs) (Mx1 and IFIT5) were increased in ALV-J infected peripheral blood lymphocytes (PBL). A significant CD8+ T cell response induced by ALV-J ap

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Zeng, Hui, Cynthia Goldsmith, Pranee Thawatsupha, et al. "Highly Pathogenic Avian Influenza H5N1 Viruses Elicit an Attenuated Type I Interferon Response in Polarized Human Bronchial Epithelial Cells." Journal of Virology 81, no. 22 (2007): 12439–49. http://dx.doi.org/10.1128/jvi.01134-07.

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ABSTRACT The unparalleled spread of highly pathogenic avian influenza A (HPAI) H5N1 viruses has resulted in devastating outbreaks in domestic poultry and sporadic human infections with a high fatality rate. To better understand the mechanism(s) of H5N1 virus pathogenesis and host responses in humans, we utilized a polarized human bronchial epithelial cell model that expresses both avian alpha-2,3- and human alpha-2,6-linked sialic acid receptors on the apical surface and supports productive replication of both H5N1 and H3N2 viruses. Using this model, we compared the abilities of selected 2004

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Gibb, David R., Emaan Madany, Najwa El Kadi, Sumaarg Pandya, Kessandra Ng, and Caroline Anne Jefferies. "Type 1 interferons promote allo-antibody responses to RBC transfusion in a lupus mouse model." Journal of Immunology 204, no. 1_Supplement (2020): 219.19. http://dx.doi.org/10.4049/jimmunol.204.supp.219.19.

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Abstract Red blood cell (RBC) transfusion exposes recipients to hundreds of unmatched minor RBC antigens. This exposure can lead to production of alloantibodies that can cause potentially fatal hemolytic events. Prior studies have reported that inflammatory states, including autoimmune disease, in the transfusion recipient can promote alloimmunization. Recent studies reported that pro-inflammatory type 1 interferons (IFNα/β) regulated RBC alloimmunization in multiple mouse transfusion models. Interestingly, patients with systemic lupus erythematosus (SLE) have an increased frequency of alloimm

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Wagner, Allison, Chi Weindel, Kelsi West, Robert Watson, and Kristin Patrick. "The splicing factor SRSF6 controls Mycobacterium tuberculosis replication through its role in maintaining mitochondrial homeostasis." Journal of Immunology 208, no. 1_Supplement (2022): 50.13. http://dx.doi.org/10.4049/jimmunol.208.supp.50.13.

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Abstract Macrophages are the primary host cell that supports the survival and replication of the intracellular bacterial pathogen Mycobacterium tuberculosis (Mtb). We are interested in how macrophage proteins are functionalized during Mtb infection. Global proteomics analysis of Mtb-infected primary macrophages found that many RNA binding proteins of the Serine/Arginine rich splicing family (SRSF) can be differentially phosphorylated, suggesting that these factors regulate splicing decisions during Mtb infection. Knockdown of one such SRSF protein, called SR6, results in basal upregulation of

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Mountz, John D., Shanrun Liu, Qi Wu, et al. "Type I IFN and IL-4R define B cell checkpoint defects in systemic lupus erythematosus." Journal of Immunology 202, no. 1_Supplement (2019): 179.5. http://dx.doi.org/10.4049/jimmunol.202.supp.179.5.

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Abstract The development of pathogenic autoantibody producing B cells is normally limited at the early transitional (Tr) stage and a later T-dependent developmental checkpoint. The precise molecular mechanisms underlying defective autoreactive B cell deletion/anergy at each checkpoint have been difficult to define. We utilized a combined single-cell B cell transcriptome and high dimensional flow cytometry analysis approach for a parallel understanding of B-cell developmental checkpoint defects at multiple stages in SLE. We found that while high levels of B-cell endogenous interferon-β (IFNβ) i

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Erlandsson, M., E. Malmhäll-Bah, K. M. Andersson, S. Töyrä Silfverswärd, R. Pullerits, and M. I. Bokarewa. "POS0702 ANTI-RHEUMATIC TREATMENT ALTERS PFKFB3 EXPRESSION, KEY OF GLYCOLYSIS, IN CD14+ MONOCYTES OF RA PATIENTS, WHICH CONTRIBUTES TO DISSIMILARITIES OF THE IFNg-SIGNATURE." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 631.1–631. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4562.

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BackgroundInterferon-gamma (IFNαnterferon-gamma (IFNRheumatology clinic, Gothenburg, Swedenh, Göteborg, Swedenmonocytes of RA patients, which contributes to dissimilarities of the IFNg-signature Peter C. Taylor Consultant of: AbbVie, Biogen, Eli Lilly and Company, Fresenius, Galapagos, mulation is energy consuming and often demands metabolic adaptation of a cell by switching glucose metabolism from the tricarboxylic acid cycle (TCA) to the pentose phosphate pathway (PPP) alternative of glycolysis that dramatically increases glucose intake. Fructose-2,6-biphosphatase 3 (coded by PFKFB3) has bee

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Netterwald, James, Shaojun Yang, Weijia Wang, et al. "Two Gamma Interferon-Activated Site-Like Elements in the Human Cytomegalovirus Major Immediate-Early Promoter/Enhancer Are Important for Viral Replication." Journal of Virology 79, no. 8 (2005): 5035–46. http://dx.doi.org/10.1128/jvi.79.8.5035-5046.2005.

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ABSTRACT Human cytomegalovirus (HCMV) infection directly initiates a signal transduction pathway that leads to activation of a large number of cellular interferon-stimulated genes (ISGs). Our previous studies demonstrated that two interferon response elements, the interferon-stimulated response element and gamma interferon-activated site (GAS), in the ISG promoters serve as HCMV response sites (VRS). Interestingly, two GAS-like VRS elements (VRS1) were also present in the HCMV major immediate-early promoter-enhancer (MIEP/E). In this study, the importance of these VRS elements in viral replica

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Borbaran Bravo, Natalia Alejandra, Ekaterina Deordieva, Larissa Doll, et al. "Autosomal Recessive COPZ1 Mutations Cause Isolated Severe Neutropenia or Complex Syndrome with Severe Neutropenia." Blood 144, Supplement 1 (2024): 417. https://doi.org/10.1182/blood-2024-199069.

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We have identified new autosomal recessive mutations in the COPZ1 gene in three severe congenital neutropenia (CN) patients from two unrelated families. In one family, two siblings with a stop-codon COPZ1 mutation (NP_057141:p.Gln141Ter) suffered from CN, lymphopenia, anemia, thrombocytopenia, and syndromic organ involvement, including hepatosplenomegaly, atypical autism with mental retardation, varying degrees of bone defects, and dermatitis. An unrelated patient with a missense COPZ1 mutation (NP_057141:p.Gly132Arg) exhibited isolated CN and chilblains. The COPZ1 gene encodes the zeta 1 subu

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Haratake, Naoki, Atrayee Bhattacharya, Ayako Nakashoji, Hiroki Ozawa, Mototsugu Shimokawa, and Donald Kufe. "Abstract 3279: MUC1 is necessary for the inflammatory memory response to osimertinib resistance in NSCLC cells." Cancer Research 84, no. 6_Supplement (2024): 3279. http://dx.doi.org/10.1158/1538-7445.am2024-3279.

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Abstract Emergence of resistance is an invariable outcome in cancer progression that may involve memory of cancer cells to treatment. The oncogenic MUC1-C protein confers pleotropic resistance of cancer cells to diverse cytotoxic and targeted agents by unclear mechanisms. We demonstrate that MUC1-C regulates the interferon (IFN) type I/II pathways in H1975 non-small cell lung cancer (NSCLC) cells selected for osimertinib resistance (H1975-OR). Targeting MUC1-C in H1975-OR cells suppressed STAT1 and inflammatory IFN signaling in association with reversing the osimertinib-resistant phenotype. St

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Dorer, D. R., M. A. Cadden, B. Gordesky-Gold, G. Harries, and A. C. Christensen. "Suppression of a lethal trisomic phenotype in Drosophila melanogaster by increased dosage of an unlinked locus." Genetics 134, no. 1 (1993): 243–49. http://dx.doi.org/10.1093/genetics/134.1.243.

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Abstract One of the most extreme examples of gene dosage sensitivity is the Triplo-lethal locus (Tpl) on the third chromosome of Drosophila melanogaster, which is lethal when present in either one or three copies. Increased dosage of an unlinked locus, Isis, suppresses the triplo-lethal phenotype of Tpl, but not the haplo-lethal phenotype. We have mapped Isis to the X chromosome region 7E3-8A5, and shown that the suppression is a gene dosage effect. Altered dosage of Isis in the presence of two copies of Tpl has no obvious effects. By examining the interactions between Isis dosage and Tpl we s

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EL Kadi, Najwa, Emaan Madany, Kessandra NG, Sumaarg Pandya, Caroline Jefferies, and David R. Gibb. "Type 1 Interferon Promotes RBC Alloimmunization in a Lupus Mouse Model." Blood 134, Supplement_1 (2019): 101. http://dx.doi.org/10.1182/blood-2019-130903.

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Background: Red blood cell (RBC) alloimmunization can follow exposure to foreign RBC antigens during transfusion therapy and during pregnancy/delivery. Alloantibodies against RBC antigens can cause potentially fatal hemolytic transfusion reactions and hemolytic disease of the newborn. Recent studies indicate that inflammatory states, including autoimmunity, promote RBC alloimmunization. For example, patients with systemic lupus erythematosus (SLE) have an elevated risk of RBC alloimmunization. Approximately 50% of SLE patients have a pro-inflammatory type 1 interferon (IFNα/β) gene signature,

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Arif, Tasleem, Kaustav Mukherjee, Li Xue, and James J. Bieker. "Sting and Vdac Inhibitors Ameliorate Ineffective Erythropoiesis in a Mouse Model of Anemia Induced By Mutation in EKLF/KLF1." Blood 144, Supplement 1 (2024): 937. https://doi.org/10.1182/blood-2024-199202.

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EKLF/Klf1 plays a vital role as a transcriptional regulator of erythroid maturation and fate specification. A semi-dominant, monoallelic point mutation of the EKLF second Zn-finger causes neonatal anemia in mice (Nan; E339D) and type IV congenital dyserythropoietic anemia in humans (CDA IV; E325K). We found that Nan/+ mutant fetal liver (FL) cells require more energy for survival and longevity, resulting in increased mitochondrial metabolism, altered mitochondrial morphology, and release of mtDNA from oxidatively stressed mitochondria, triggering an elevated inflammatory response through activ

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Poddar, Soumya, Jiali Yan, Gayatri Tiwari, et al. "Impact of Inflammation, Tumor and Product Attributes on Clinical Outcomes in Patients with Relapsed/Refractory Follicular Lymphoma Treated with Axicabtagene Ciloleucel." Blood 144, Supplement 1 (2024): 4368. https://doi.org/10.1182/blood-2024-211139.

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Background: The ZUMA-5 trial, investigating axicabtagene ciloleucel (axi-cel), an anti-CD19 CAR T cell therapy, in third-line indolent-NHL, demonstrated high rate of durable response with a manageable safety profile (Jacobson et al., Lancet Oncology 2022). Results from this trial led to the approval of axi-cel in relapsed/refractory (r/r) Follicular Lymphoma (FL) patients. While clinical outcomes were remarkable, biomarkers associated with efficacy and high-grade toxicity in r/r FL patients treated with axi-cel are not well established. Methods: This report presents univariate and multivariate

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Thomas, Brian J., Xue Bai, Benjamin J. Cryer, Mark A. Daniels, Margaret J. Lange, and Donald H. Burke. "Abstract 7298: DUSP11 is an intracellular innate immune checkpoint in lung adenocarcinoma." Cancer Research 85, no. 8_Supplement_1 (2025): 7298. https://doi.org/10.1158/1538-7445.am2025-7298.

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Abstract The major success of immune checkpoint inhibitors (ICIs) to treat cancer highlights both the efficacy of inhibiting immunosuppressive proteins as a means of re-activating the anti-tumor immune response and the generalizability of targeting such proteins (i.e., therapies are clinically useful across many cancer types). While the major focus in immuno-oncology has been to manipulate the adaptive immune system, recent attention has been given to manipulating the innate immune system to treat cancer and/or enhance adaptive responses. In this work we detail the intracellular protein, Dual

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Salari, Kiarash, Matthew Wells, Eleanor R. Johnson, et al. "Abstract 675: Understanding SETDB1-mediated tumor immune evasion mechanism in endometrial cancer." Cancer Research 83, no. 7_Supplement (2023): 675. http://dx.doi.org/10.1158/1538-7445.am2023-675.

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Abstract SETDB1 is characterized as an important epigenetic regulator in many different cancers and involved in transcriptional silencing of many different processes and pathways. It is often overexpressed in many different cancers including colon, melanoma, breast and pancreatic cancers and its high expression is correlated with worse patient outcome. Often associated with repressing complexes such as HUSH and KAP1/KRAB, it has been shown to repress many different genes such as p53 and p21 through histone H3K9 methylation. In addition, it has been implicated in regulating transposable element

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Huschka, Henriette, and Sabine Mihm. "Hepatic IFNL4 Gene Activation in Hepatocellular Carcinoma Patients with Regard to Etiology." International Journal of Molecular Sciences 22, no. 15 (2021): 7803. http://dx.doi.org/10.3390/ijms22157803.

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Hepatocellular carcinoma (HCC) is a malignancy with a leading lethality. The etiology is quite diverse, ranging from viral infections to metabolic disorders or intoxications, and associates with specific somatic mutational patterns and specific host immunological phenotypes. Particularly, hepatitis C virus (HCV)-infected liver is featured by an activation of interferon (IFN)-stimulated genes (ISGs; IFN signature), which we suppose is driven by type III IFNL4. Taking advantage of the TCGA collection of HCC patients of various different etiologies, this study aimed at validating our previous fin

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You, Eunae, Luli Zou, Patrick Danaher, et al. "Abstract C038: Repeat RNA dysregulation of cellular states in the pancreatic cancer microenvironment." Cancer Research 82, no. 22_Supplement (2022): C038. http://dx.doi.org/10.1158/1538-7445.panca22-c038.

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Abstract Aberrant transcription of the repeat RNAs is a common feature in epithelial cancers including PDAC, but the function of these non-coding RNAs in cancer development is relatively unexplored. We have found that these repeat RNAs are sensed and replicate like retroviruses, and now have identified the ability of these viral-like elements to be transmitted from cancer cells through extracellular vesicles (EVs). PDAC-derived EVs applied to cancer-associated fibroblasts (CAFs) activates interferon-stimulated genes (ISGs) and is able to drive CAFs towards an inflammatory CAF (iCAF) phenotype

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Johnson, Deborah C., Mihaela-Carmen Unciuleac, and Dennis R. Dean. "Controlled Expression and Functional Analysis of Iron-Sulfur Cluster Biosynthetic Components within Azotobacter vinelandii." Journal of Bacteriology 188, no. 21 (2006): 7551–61. http://dx.doi.org/10.1128/jb.00596-06.

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ABSTRACT A system for the controlled expression of genes in Azotobacter vinelandii by using genomic fusions to the sucrose catabolic regulon was developed. This system was used for the functional analysis of the A. vinelandii isc genes, whose products are involved in the maturation of [Fe-S] proteins. For this analysis, the scrX gene, contained within the sucrose catabolic regulon, was replaced by the contiguous A. vinelandii iscS, iscU, iscA, hscB, hscA, fdx, and iscX genes, resulting in duplicate genomic copies of these genes: one whose expression is directed by the normal isc regulatory ele

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Ho, Manh Tin, Jiongming Lu, Paula Vazquez-Pianzola та Beat Suter. "α-Phenylalanyl tRNA synthetase competes with Notch signaling through its N-terminal domain". PLOS Genetics 18, № 4 (2022): e1010185. http://dx.doi.org/10.1371/journal.pgen.1010185.

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The alpha subunit of the cytoplasmic Phenylalanyl tRNA synthetase (α-PheRS, FARSA in humans) displays cell growth and proliferation activities and its elevated levels can induce cell fate changes and tumor-like phenotypes that are neither dependent on the canonical function of charging tRNAPhe with phenylalanine nor on stimulating general translation. In intestinal stem cells of Drosophila midguts, α-PheRS levels are naturally slightly elevated and human FARSA mRNA levels are elevated in multiple cancers. In the Drosophila midgut model, elevated α-PheRS levels caused the accumulation of many a

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Kumar, Santosh, Shubhankar Suman, Jerry Angdisen, et al. "Effects of High-Linear-Energy-Transfer Heavy Ion Radiation on Intestinal Stem Cells: Implications for Gut Health and Tumorigenesis." Cancers 16, no. 19 (2024): 3392. http://dx.doi.org/10.3390/cancers16193392.

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Heavy ion radiation, prevalent in outer space and relevant for radiotherapy, is densely ionizing and poses a risk to intestinal stem cells (ISCs), which are vital for maintaining intestinal homeostasis. Earlier studies have shown that heavy-ion radiation can cause chronic oxidative stress, persistent DNA damage, cellular senescence, and the development of a senescence-associated secretory phenotype (SASP) in mouse intestinal mucosa. However, the specific impact on different cell types, particularly Lgr5+ intestinal stem cells (ISCs), which are crucial for maintaining cellular homeostasis, GI f

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Zhou, Jianbiao, Jonathan Adam Scolnick, Stacy Xu, et al. "Single-Cell Multi-Omic Analysis Uncovers Comprised Immune Function and Primary Resistance Mechanism in Acute Myeloid Leukemia." Blood 138, Supplement 1 (2021): 378. http://dx.doi.org/10.1182/blood-2021-149022.

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Abstract Background: Approximately 20% of AML patients do not respond to induction chemotherapy (primary resistance) and 40-60% of patients develop secondary resistance, eventually leading to relapse followed by refractory disease (RR-AML). Diversified molecular mechanisms have been proposed for drug resistance and RR phenotype. However, we still cannot predict when relapse will occur, nor which patients will become resistant to therapy. Single-cell multi-omic (ScMo) profiling may provide new insights into our understanding of hematopoietic stem cell (HSC) differentiation trajectories, tumor h

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Amcheslavsky, Alla, Naoto Ito, Jin Jiang, and Y. Tony Ip. "Tuberous sclerosis complex and Myc coordinate the growth and division of Drosophila intestinal stem cells." Journal of Cell Biology 193, no. 4 (2011): 695–710. http://dx.doi.org/10.1083/jcb.201103018.

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Intestinal stem cells (ISCs) in the adult Drosophila melanogaster midgut can respond to damage and support repair. We demonstrate in this paper that the tuberous sclerosis complex (TSC) plays a critical role in balancing ISC growth and division. Previous studies have shown that imaginal disc cells that are mutant for TSC have increased rates of growth and division. However, we report in this paper that loss of TSC in the adult Drosophila midgut results in the formation of much larger ISCs that have halted cell division. These mutant ISCs expressed proper stem cell markers, did not differentiat

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Kim, Eunha, Jenny Lai, Yanyi Sun, et al. "Homeostatic Type I IFN Response at the Placenta Contributes to Sex-biased Neurodevelopmental Outcome." Journal of Immunology 212, no. 1_Supplement (2024): 1207_4712. http://dx.doi.org/10.4049/jimmunol.212.supp.1207.4712.

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Abstract The maternal-fetal interface, placenta, plays pivotal roles in fetal development. Recent evidence shows that the placenta contributes to the sex-biased prevalence of some developmental disorders such as neurodevelopmental disorders. Commencing an exploration into the molecular intricacies of fetal sex-specific transcriptional changes within the placenta, our study leveraged single-cell RNA sequencing. We uncovered a diminished expression of interferon (IFN)-responsive genes (ISGs) in male fetus-associated trophoblasts compared to female, which have pivotal roles in the process of spir

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