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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Cao, Yanhong, Lishi Wang, Cong-Yi Wang, Jicheng Ye, Ying Wang, Tiantian Li, Franklin Garcia-Godoy, Dianjun Sun, Weikuan Gu, and Arnold E. Postlethwaite. "Sex Differences in Correlation with Gene Expression Levels between Ifi200 Family Genes and Four Sets of Immune Disease-Relevant Genes." Journal of Immunology Research 2018 (August 28, 2018): 1–12. http://dx.doi.org/10.1155/2018/1290814.

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Background. The HIN-200 family genes in humans have been linked to several autoimmune diseases—particularly to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Recently, its human counterpart gene cluster, the Ifi200 family in mice, has been linked to spontaneous arthritis disease (SAD). However, many immune-mediated diseases (including RA and SLE) show gender difference. Understanding whether or not and how these genes play a role in sex difference in immune-mediated diseases is essential for diagnosis/treatment. Methods. This study takes advantage of the whole genome gene expression profiles of recombinant inbred (RI) strain populations from female and male mice to analyze potential sex differences in a variety of genes in disease pathways. Expression levels and regulatory QTL of Ifi200 family genes between female and male mice were first examined in a large mouse population, including RI strains derived from C57BL/6J, DBA/2J (BXD), and classic inbred strains. Sex similarities and differences were then analyzed for correlations with gene expression levels between genes in the Ifi200 family and four selected gene sets: known immune Ifi200 pathway-related genes, lupus-relevant genes, osteoarthritis- (OA-) and RA-relevant genes, and sex hormone-related genes. Results. The expression level of Ifi202b showed the most sex difference in correlation with known immune-related genes (the P value for Ifi202b is 0.0004). Ifi202b also showed gender difference in correlation with selected sex hormone genes, with a P value of 0.0243. When comparing coexpression levels between Ifi200 genes and lupus-relevant genes, Ifi203 and Ifi205 showed significant sex difference (P values: 0.0303 and 0.002, resp.). Furthermore, several key genes (e.g., Csf1r, Ifnb1, IL-20, IL-22, IL-24, Jhdm1d, Csf1r, Ifnb1, IL-20, IL-22, IL-24, and Tgfb2 that regulate sex differences in immune diseases) were discovered. Conclusions. Different genes in the Ifi200 family play different roles in sex difference among dissimilar pathways of these four gene groups.

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Zhang, Ke, Daniel Kagan, Wendy DuBois, Richard Robinson, Valery Bliskovsky, William C. Vass, Shuling Zhang, and Beverly A. Mock. "Mndal, a new interferon-inducible family member, is highly polymorphic, suppresses cell growth, and may modify plasmacytoma susceptibility." Blood 114, no. 14 (October 1, 2009): 2952–60. http://dx.doi.org/10.1182/blood-2009-01-198812.

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The human HIN-200 gene cluster and its mouse counterpart, the interferon inducible-200 (Ifi200) family, both on Chr 1, are associated with several diseases, including solid tumors and lupus. Our study was initiated to identify the modifier gene(s) encoded by the Pctm locus, in which mouse B-cell plasmacytomas induced by pristane are associated with heterozygosity of Chr 1 genes near the Ifi200 cluster. A screen for differentially expressed genes in granulomatous tissues induced by pristane in resistant and susceptible strains identified a new Ifi200 member whose expression was 1000-fold higher in the strain carrying the resistant allele of Pctm and was the most highly expressed Ifi200 gene. The gene, designated Mndal (for MNDA-like, myeloid nuclear differentiation antigen-like), was absent in the susceptible genome, as were genomic sequences upstream of Ifi203, the gene adjacent to Mndal. Ectopic expression of MNDAL suppressed cell growth, which, together with the disease susceptibility of heterozygotes at the Pctm locus, suggests that Mndal, perhaps with Ifi203, acts as a tumor suppressor and display(s) haploinsufficiency. Mndal is highly polymorphic among inbred mouse strains, because it is absent in 10 of 24 strains. This polymorphism may have implications for other disease modifiers mapping to the same region.

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Wang, H., G. Chatterjee, J. J. Meyer, C.-J. Liu, N. A. Manjunath, P. Bray-Ward, and P. Lengyel. "Characteristics of Three Homologous 202 Genes (Ifi202a, Ifi202b, and Ifi202c) from the Murine Interferon-Activatable Gene 200 Cluster." Genomics 60, no. 3 (September 1999): 281–94. http://dx.doi.org/10.1006/geno.1999.5923.

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4

Ghosh, Sreya, Susan Carpenter, and Katherine Fitzgerald. "The PYHIN family member IFI205 regulates immune signaling via transcriptional regulation of the inflammasome adapter ASC (P1280)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 116.18. http://dx.doi.org/10.4049/jimmunol.190.supp.116.18.

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Abstract Members of the PYHIN protein family such as AIM2 and IFI16, function as DNA sensors in innate immunity. Here we investigated the role of Ifi205, a murine PYHIN family member in innate immunity by generating murine macrophages lacking Ifi205 and monitoring immune signaling in these cells. Macrophages lacking Ifi205 had abrogated caspase-1 dependent processing and production of the pro-inflammatory cytokine IL-1β in response to cytosolic double stranded DNA and Nigericin, that activate the AIM2 and NLRP3 inflammasomes, respectively. Surprisingly, expression of the inflammasome adapter ASC was completely abolished at both the protein and mRNA levels in all Ifi205 knockdown cells generated. Reconstitution of the knockdown cells with ASC rescued IL-1β production attributing the knockdown phenotype to the loss of ASC expression. We observed a similar defect in ASC expression in cell lines lacking Ifi205 by targeting the 3’-UTR of the ifi205 gene. Reconstitution of these cells with Ifi205 rescued ASC mRNA expression. We also found that ectopic expression of Ifi205 augmented the activation of an ASC promoter-luciferase reporter gene in a dose-dependent manner in HEK 293T cells. The data suggest that ASC expression might be controlled at the transcriptional level. Thus, Ifi205 regulates inflammasome activation by controlling transcriptional regulation of ASC.

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5

Li, Tuoyang, Junyi Zhou, Yingming Jiang, Yandong Zhao, Jintuan Huang, Weiyao Li, Zhenze Huang, et al. "The Novel Protein ADAMTS16 Promotes Gastric Carcinogenesis by Targeting IFI27 through the NF-κb Signaling Pathway." International Journal of Molecular Sciences 23, no. 19 (September 20, 2022): 11022. http://dx.doi.org/10.3390/ijms231911022.

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A disintegrin and metalloproteinase with thrombospondin motifs 16 (ADAMTS16) has been reported to be involved in the pathogenesis of solid cancers. However, its role in gastric cancer (GC) is unclear. In this study, the role of ADAMTS16 in gastric cancer was investigated. The effects of ADAMTS16 on cell migration, invasion, and proliferation were investigated by functional experiments in vivo and in vitro. Downstream signal pathways of ADAMTS16 were confirmed by using bioinformatics analysis, co-immunoprecipitation, and immunofluorescence. Meanwhile, bioinformatics analysis, qRT-PCR, western blot, and dual-luciferase reporter gene analysis assays were used to identify ADAMTS16 targets. The expression of ADAMTS16 in GC was analyzed in public datasets. The expression of ADAMTS16 and its correlations with the clinical characteristics of GC were investigated by immunohistochemistry. Ectopic ADAMTS16 expression significantly promoted tumor cell migration, invasion, and growth. Bioinformatics analysis and western blot showed that ADAMTS16 upregulated the IFI27 protein through the NF-κb pathway, which was confirmed by immunofluorescence and western blot. Dual-luciferase reporter gene analysis identified a binding site between P65 and IFI27 that may be directly involved in the transcriptional regulation of IFI27. IFI27 knockdown reversed the promoting effect of ADAMTS16 on cell invasion, migration, and proliferation indicating that ADAMTS16 acts on GC cells by targeting the NF-κb/IFI27 axis. ADAMTS16 was associated with poor prognosis in clinical characteristics. ADAMTS16 promotes cell migration, invasion, and proliferation by targeting IFI27 through the NF-κB pathway and is a potential progressive and survival biomarker of GC.

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6

Xu, Lin, Tingjian Zu, Tao Li, Min Li, Jun Mi, Fuxiang Bai, Guanyi Liu, et al. "ATF3 downmodulates its new targets IFI6 and IFI27 to suppress the growth and migration of tongue squamous cell carcinoma cells." PLOS Genetics 17, no. 2 (February 4, 2021): e1009283. http://dx.doi.org/10.1371/journal.pgen.1009283.

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Activating transcription factor 3 (ATF3) is a key transcription factor involved in regulating cellular stress responses, with different expression levels and functions in different tissues. ATF3 has also been shown to play crucial roles in regulating tumor development and progression, however its potential role in oral squamous cell carcinomas has not been fully explored. In this study, we examined biopsies of tongue squamous cell carcinomas (TSCCs) and found that the nuclear expression level of ATF3 correlated negatively with the differentiation status of TSCCs, which was validated by analysis of the ATGC database. By using gain- or loss- of function analyses of ATF3 in four different TSCC cell lines, we demonstrated that ATF3 negatively regulates the growth and migration of human TSCC cells in vitro. RNA-seq analysis identified two new downstream targets of ATF3, interferon alpha inducible proteins 6 (IFI6) and 27 (IFI27), which were upregulated in ATF3-deleted cells and were downregulated in ATF3-overexpressing cells. Chromatin immunoprecipitation assays showed that ATF3 binds the promoter regions of the IFI6 and IFI27 genes. Both IFI6 and IFI27 were highly expressed in TSCC biopsies and knockdown of either IFI6 or IFI27 in TSCC cells blocked the cell growth and migration induced by the deletion of ATF3. Conversely, overexpression of either IFI6 or IFI27 counteracted the inhibition of TSCC cell growth and migration induced by the overexpression of ATF3. Finally, an in vivo study in mice confirmed those in vitro findings. Our study suggests that ATF3 plays an anti-tumor function in TSCCs through the negative regulation of its downstream targets, IFI6 and IFI27.

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7

KIMOTO, OSAMU, JIN SAWADA, KUMIKO SHIMOYAMA, DAISUKE SUZUKI, SATOKI NAKAMURA, HIDEHARU HAYASHI, and NORIYOSHI OGAWA. "Activation of the Interferon Pathway in Peripheral Blood of Patients with Sjögren’s Syndrome." Journal of Rheumatology 38, no. 2 (November 15, 2010): 310–16. http://dx.doi.org/10.3899/jrheum.100486.

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Objective.DNA microarray analysis and quantitative real-time polymerase chain reaction (PCR) were performed to identify key target genes in peripheral blood from patients with Sjögren’s syndrome (SS).Methods.DNA microarray analysis was performed in 19 patients with SS (all women) and 10 healthy controls (5 men and 5 women) using a low-density DNA microarray system with 778 genes. For confirmation, the expression of upregulated genes was analyzed by quantitative real-time PCR in another 37 SS patients (35 women and 2 men) and 9 healthy controls (8 women and 1 man). Relationships between gene signatures and various clinical measures, such as disease duration, symptoms and signs, complications, immunological findings, and salivary and lacrimal functions, were analyzed.Results.Interferon-α (IFN-α)-inducible protein 27 (IFI27) showed the most significant difference between SS patients and controls in the microarray screening. We performed quantitative RT-PCR for IFI27. IFI27 gene expression level was increased in patients with SS compared with controls (p < 0.01) by real-time PCR, supporting our observations from the microarray data. The level of IFI27 was significantly correlated with serum IgG levels (r = 0.462, p < 0.01) and ß2-microglobulin (r = 0.385, p < 0.05), soluble interleukin 2 receptor (r = 0.473, p < 0.01), erythrocyte sedimentation rate (r = 0.333, p < 0.05), and antinuclear antibody titer (speckled pattern; r = 0.445, p < 0.01).Conclusion.Our results suggest that upregulation of IFN-inducible genes in SS patients is a systemic phenomenon, and IFN may play an important role in the pathogenesis of SS. The expression level of IFI27 could be an effective and specific biomarker associated with SS.

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Lei, Hongxing. "A two-gene marker for the two-tiered innate immune response in COVID-19 patients." PLOS ONE 18, no. 1 (January 17, 2023): e0280392. http://dx.doi.org/10.1371/journal.pone.0280392.

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For coronavirus disease 2019 (COVID-19), a pandemic disease characterized by strong immune dysregulation in severe patients, convenient and efficient monitoring of the host immune response is critical. Human hosts respond to viral and bacterial infections in different ways, the former is characterized by the activation of interferon stimulated genes (ISGs) such as IFI27, while the latter is characterized by the activation of anti-bacterial associated genes (ABGs) such as S100A12. This two-tiered innate immune response has not been examined in COVID-19. In this study, the activation patterns of this two-tiered innate immune response represented by IFI27 and S100A12 were explored based on 1421 samples from 17 transcriptome datasets derived from the blood of COVID-19 patients and relevant controls. It was found that IFI27 activation occurred in most of the symptomatic patients and displayed no correlation with disease severity, while S100A12 activation was more restricted to patients under severe and critical conditions with a stepwise activation pattern. In addition, most of the S100A12 activation was accompanied by IFI27 activation. Furthermore, the activation of IFI27 was most pronounced within the first week of symptom onset, but generally waned after 2–3 weeks. On the other hand, the activation of S100A12 displayed no apparent correlation with disease duration and could last for several months in certain patients. These features of the two-tiered innate immune response can further our understanding on the disease mechanism of COVID-19 and may have implications to the clinical triage. Development of a convenient two-gene protocol for the routine serial monitoring of this two-tiered immune response will be a valuable addition to the existing laboratory tests.

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9

Tang, Benjamin M., Maryam Shojaei, Grant P. Parnell, Stephen Huang, Marek Nalos, Sally Teoh, Kate O'Connor, et al. "A novel immune biomarker IFI27 discriminates between influenza and bacteria in patients with suspected respiratory infection." European Respiratory Journal 49, no. 6 (June 2017): 1602098. http://dx.doi.org/10.1183/13993003.02098-2016.

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Host response biomarkers can accurately distinguish between influenza and bacterial infection. However, published biomarkers require the measurement of many genes, thereby making it difficult to implement them in clinical practice. This study aims to identify a single-gene biomarker with a high diagnostic accuracy equivalent to multi-gene biomarkers.In this study, we combined an integrated genomic analysis of 1071 individuals with in vitro experiments using well-established infection models.We identified a single-gene biomarker, IFI27, which had a high prediction accuracy (91%) equivalent to that obtained by multi-gene biomarkers. In vitro studies showed that IFI27 was upregulated by TLR7 in plasmacytoid dendritic cells, antigen-presenting cells that responded to influenza virus rather than bacteria. In vivo studies confirmed that IFI27 was expressed in influenza patients but not in bacterial infection, as demonstrated in multiple patient cohorts (n=521). In a large prospective study (n=439) of patients presented with undifferentiated respiratory illness (aetiologies included viral, bacterial and non-infectious conditions), IFI27 displayed 88% diagnostic accuracy (AUC) and 90% specificity in discriminating between influenza and bacterial infections.IFI27 represents a significant step forward in overcoming a translational barrier in applying genomic assay in clinical setting; its implementation may improve the diagnosis and management of respiratory infection.

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10

Wieland, Karen, Andrew Woo, Thomas Akie, and Alan B. Cantor. "Increased Interferon-αa Signaling During Megakaryocyte Ontogeny: Implications for the Spontaneous Resolution of Down Syndrome Transient Myeloproliferative Disorder." Blood 114, no. 22 (November 20, 2009): 1272. http://dx.doi.org/10.1182/blood.v114.22.1272.1272.

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Abstract Abstract 1272 Poster Board I-294 About ten percent of infants with Down syndrome (DS) are born with a transient myeloproliferative disorder (DS-TMD), which spontaneously resolves within the first few months of life. However, the basis for this resolution remains unknown. Acquired mutations leading to exclusive production of a short isoform of the transcription factor GATA-1 (GATA-1s) occur in all cases of DS-TMD, and knock-in mice that exclusively produce GATA-1s have hyperproliferation of megakaryocytes during early fetal liver hematopoiesis, but not during later developmental stages. In this study, we found striking upregulation of the interferon-αa (IFN-αa) receptor and multiple IFN-αa responsive genes, including Ifi203, Ifi205, Irf-1, Irf-8, and Ifitm6, in immunophenotypically isolated megakaryocyte progenitor cells (MkPs) from bone marrow versus embryonic day 13.5 (e13.5) fetal liver of wild type mice. These differences were confirmed at the protein level in megakaryocytes by in situ immunohistochemistry. Addition of IFN-αa to GATA-1s containing e13.5 fetal liver MkPs reduces their hyperproliferation in vitro in a dose-dependent manner. Conversely, injection of neutralizing IFN-αa/β antibodies, but not control IgG, into adult GATA-1s mice markedly increases the percentage of bone marrow CD41+ cells and morphologically recognizable megakaryocytes, in contrast to wild type mice. We propose that increases in IFN-αa signaling during megakaryocyte ontogeny may account for the developmental stage-specific effects of GATA-1s on megakaryocyte hyperproliferation, and possibly the spontaneous resolution of DS-TMD. Interestingly, the genes encoding the IFN-αa/β receptor are located on human chromosome 21 and are expressed at 1.6 times that in trisomy versus disomy 21 cells. We speculate that increased interferon alpha signaling during embryogenesis may be the basis for the strong selective pressure for GATA-1s producing mutations in trisomy 21 fetuses in the first place. Disclosures No relevant conflicts of interest to declare.

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11

Choubey, Divaker, and Ravichandran Panchanathan. "Interferon-inducible Ifi200-family genes in systemic lupus erythematosus." Immunology Letters 119, no. 1-2 (August 2008): 32–41. http://dx.doi.org/10.1016/j.imlet.2008.06.001.

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12

Subramanian, Gayatri, Ritu Chakravarti, and Saurabh Chattopadhyay. "Ifi204/p204, a new piece in the sepsis puzzle." Annals of Translational Medicine 6, S1 (November 2018): S12. http://dx.doi.org/10.21037/atm.2018.09.22.

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Lao, Mengyi, Xiaozhen Zhang, Tao Ma, Jian Xu, Hanshen Yang, Yi Duan, Honggang Ying, et al. "Regulator of calcineurin 1 gene isoform 4 in pancreatic ductal adenocarcinoma regulates the progression of tumor cells." Oncogene 40, no. 17 (April 6, 2021): 3136–51. http://dx.doi.org/10.1038/s41388-021-01763-z.

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AbstractTherapeutic strategies to treat pancreatic ductal adenocarcinoma (PDAC) remain unsatisfying and limited. Therefore, it is imperative to fully determine the mechanisms underlying PDAC progression. In the present study, we report a novel role of regulator of calcineurin 1, isoform 4 (RCAN1.4) in regulating PDAC progression. We demonstrated that RCAN1.4 expression was decreased significantly in PDAC tissues compared with that in para-cancerous tissues, and correlated with poor prognosis of patients with pancreatic cancer. In vitro, stable high expression of RCAN1.4 could suppress the metastasis and proliferation and angiogenesis of pancreatic tumor cells. In addition, interferon alpha inducible protein 27 (IFI27) was identified as having a functional role in RCAN1.4-mediated PDAC migration and invasion, while VEGFA play a vital role in RCAN1.4-mediated PDAC angiogenesis. Analysis of mice with subcutaneously/orthotopic implanted xenograft tumors and liver metastasis model confirmed that RCAN1.4 could modulate the growth, metastasis, and angiogenesis of tumors via IFI27/VEGFA in vivo. In conclusion, our results suggested that RCAN1.4 suppresses the growth, metastasis, and angiogenesis of PDAC, functioning partly via IFI27 and VEGFA. Importantly, our results provided possible diagnostic criteria and therapeutic targets for PDAC.

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Choubey, Divaker. "Interferon-inducible Ifi200-family genes as modifiers of lupus susceptibility." Immunology Letters 147, no. 1-2 (September 2012): 10–17. http://dx.doi.org/10.1016/j.imlet.2012.07.003.

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15

Huang, Huijuan, Jiannan Lv, Yonglun Huang, Zhiyi Mo, Haisheng Xu, Yiyang Huang, Linghui Yang, Zhengqiu Wu, Hongmian Li, and Yaqin Qin. "IFI27 is a potential therapeutic target for HIV infection." Annals of Medicine 54, no. 1 (January 22, 2022): 314–25. http://dx.doi.org/10.1080/07853890.2021.1995624.

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LI, Y. N., C. W. Chen, T. Trinh-Minh, Z. Honglin, P. Hubel, J. Pfannstiel, G. Schett, and J. H. W. Distler. "POS0344 O-GlcNAcylation ON NUP153 REGULATES THE EARLY STAGES OF OSTEOCLASTOGENESIS THROUGH MYC NUCLEAR TRANSLOCATION." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 426.1–426. http://dx.doi.org/10.1136/annrheumdis-2022-eular.1161.

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BackgroundBone homeostasis is maintained by the balance between bone formation and resorption. In inflammatory arthritis, such as rheumatoid arthritis (RA), the pro-inflammatory environment promotes osteoclast differentiation and skews this balance towards bone resorption, leading to destructive bone erosion and bone loss. O-GlcNAcylation is one of the most common post-translational modifications, which attaches a single N-acetylglucosamine (GlcNAc) molecular to the serine or threonine of the target protein. O-GlcNAcylation is controlled by the activities of a single pair of enzymes: OGT, which facilitates the transfer of GlcNAc onto proteins; OGA, which removes GlcNAc from proteins. The activity of O-GlcNAcylation has been reported to be involved in several cellular events, such as transcription, translation, intracellular trafficking, and differentiation. We previously showed that the dynamics of O-GlcNAcylation are essential for osteoclast differentiation. TNF-α, a key pro-inflammatory factor in RA, intensified the O-GlcNAcylation dynamics. Inhibition of OGT arrests osteoclast precursors at early stages, whereas OGA inhibition blocks osteoclast maturation. However, the molecular mechanism of these regulations remains unclear.ObjectivesWe aimed to identify the O-GlcNAcylation targets in osteoclast precursors in a pro-inflammatory milieu and to decipher the molecular mechanism of O-GlcNAcylation mediated regulation of osteoclastogenesis.MethodsWe first identify the O-GlcNAc-dependent molecular pathways in osteoclast precursors with pharmacological OGT and OGA inhibition by RNA sequencing. Then, we identified the O-GlcNAcylated proteins by mass spectrometry-based proteomics analysis and confirmed by immunoprecipitation. We found the potential molecular mechanism by combining the data from transcriptomics and proteomics. The proposed mechanism was further validated through siRNA-mediated knockdown and high-content screening analysis.ResultsOur transcriptomics data showed that OGT inhibition arrested osteoclast differentiation at early stages through interfering the cytokine signaling and metabolic adaption. The upstream analysis proposed MYC as the most potent regulator for the transcriptomic profile under OGT inhibition. Recent studies proposed MYC as a master regulator for metabolic reprograming during osteoclast differentiation. However, O-GlcNAcylation of MYC was not detected by mass spectrometry, suggesting indirect effects of O-GlcNAcylation on MYC signaling in osteoclast precursors. We detected upregulated levels of O-GlcNAc on NUP153, MTDH, RBM27, IFI207 upon RANKL+TNFα stimulation. An integrated analysis of transcriptomic and proteomic data by Ingenuity Pathway Analysis indicated that NUP153 might regulate the most DEGs among all the identified targets and indicated potential of NUP153 to regulate nuclear shuttling of MYC. Subcellular fractionation and confocal microscopy showed enhanced MYC nuclear translocation upon RANKL+TNFα stimulation, which could be blocked by NUP153 knockdown or OGT inhibition. Functionally, knockdown of NUP153 arrested cells at similar stages to OGT inhibition and reduced bone resorption ability. Together, these results suggest a model, in which O-GlcNAcylation regulates the shuttling activity of the nuclear pore component NUP153 to control the access of MYC to the nucleus during osteoclast differentiation.ConclusionOur results indicated that OGT inhibition arrests osteoclastogenesis at early stages through hampering MYC-dependent metabolic adaption. NUP153 was proposed as the most potent O-GlcNAcylation target by multi-omics data integration. NUP153-mediated MYC nuclear trafficking is required for osteoclast differentiation. These findings reveal the molecular mechanism of O-GlcNAcylation-dependent osteoclastogenesis and provide therapeutic insights on targeting O-GlcNAcylation in pathologic bone resorption.Disclosure of InterestsYi-Nan Li: None declared, Chih-Wei Chen: None declared, Thuong Trinh-Minh: None declared, ZHU Honglin: None declared, Philipp Hubel: None declared, Jens Pfannstiel: None declared, Georg Schett: None declared, Jörg H.W. Distler Shareholder of: 4D Science, Speakers bureau: Boehringer Ingelheim, Paid instructor for: Boehringer Ingelheim, Consultant of: Actelion, Active Biotech, Anamar, ARXX, Bayer Pharma, Boehringer Ingelheim, Celgene, Galapagos, GSK, Inventiva, JB Therapeutics, Medac, Pfizer, RuiYi and UCB, Grant/research support from: Anamar, Active Biotech, Array Biopharma, aTyr, BMS, Bayer Pharma, Boehringer Ingelheim, Celgene, Galapagos, GSK, Inventiva, Novartis, Sanofi-Aventis, RedX, UCB, Employee of: FibroCure

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KIMKONG, INGORN, YINGYOS AVIHINGSANON, and NATTIYA HIRANKARN. "Association of IFI200 Gene Polymorphisms with Susceptibility to Systemic Lupus Erythematosus." Journal of Rheumatology 37, no. 7 (July 2010): 1544.2–1547. http://dx.doi.org/10.3899/jrheum.091255.

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Jin, Weiwei, Wenfang Jin, and Dongning Pan. "Ifi27 is indispensable for mitochondrial function and browning in adipocytes." Biochemical and Biophysical Research Communications 501, no. 1 (June 2018): 273–79. http://dx.doi.org/10.1016/j.bbrc.2018.04.234.

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Singh, Ram, Ravi Dinesh, and Bevra Hahn. "Role of IFI202b in the suppressive ability of CD8+Treg induced in (NZB x NZW) F1 lupus mice (143.56)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 143.56. http://dx.doi.org/10.4049/jimmunol.184.supp.143.56.

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Abstract Tolerance with an artificial peptide (pConsensus, pCons) based on anti-DNA IgG sequences containing MHC class I and class II T cell determinants, causes NZB/NZW F1 female (BWF1) mice to develop CD8+Foxp3+ inhibitory T (Ti) cells which suppress anti-DNA Ig production. CD8+T cells from mice tolerized with pCons expressed Ifi202b more than two-fold higher than cells from untolerized mice, with an increase 1-4 weeks after tolerization and a return toward baseline at 6 weeks. In vitro polyclonal activation significantly increased Ifi202b mRNA expression in tolerized CD8+T cells. Importantly, silencing of Ifi202b abrogated the suppressive capacity of tolerized CD8+T cells. This was associated with decreased expression of Foxp3, and decreased gene and protein expression of TGFb, but not of IL-2, IFN-g, IL-10 or IL-17. These changes were not related with resistance to apoptosis induced in CD8+Treg. Although Ifi202b is induced by interferons, silencing of another IFN-induced gene upregulated in tolerized CD8+T cells, IFNar1, had no effect on the ability of CD8+T cells to suppress autoantibody production. Taken together, these data identify a role for Ifi202b in the suppressive capacity of peptide-induced regulatory CD8+T cells via effects on the expression of Foxp3 and the synthesis of TGFb.

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Turaga, Soumya, Daniel Silver, Evi Paouri, Defne Bayik, Sen Peng, James Connor, Jill Barnholtz-Sloan, et al. "TMIC-02. JUNCTIONAL ADHESION MOLECULE-A (JAM-A) DEFICIENCY DRIVES SEX-SPECIFIC DIFFERENCES IN GLIOBLASTOMA PROGRESSION VIA DIFFERENTIAL MICROGLIA RESPONSES IN THE TUMOR MICROENVIRONMENT." Neuro-Oncology 21, Supplement_6 (November 2019): vi247. http://dx.doi.org/10.1093/neuonc/noz175.1036.

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Abstract Despite the male preponderance for developing glioblastoma (GBM) and better survival outcomes in females, current treatment paradigms do not account for biological sex as a biological or clinical variable. Sex-specific molecular alterations that drive tumor cell growth and therapy response have been documented, however, sex-specific extrinsic differences in the tumor microenvironment have yet to be identified. Based on well-established sex-specific gene signatures and functional differences in microglia, we interrogated influences of male and female microglia in driving GBM growth. Specifically, manipulation of JAM-A expression, a tight junction protein on microglia, was exploited as a paradigm for determining effects on in vivo syngeneic GBM mouse models. Male and female JAM-A KO mice that received orthotopic injection of syngeneic GBM cells presented differential overall survival distinct from their wildtype counterparts. Wild-type male mice phenocopied human males, presenting shorter overall survival than females, this trend was reversed in JAM-A KO mice. Compared to the other genotypes, female JAM-A KO mice presented the greatest number of phagocytic, tumor-promoting, activated microglia. RNA-sequencing of tumors from JAM-A KO and WT mice revealed that female JAM-A KO mice had increased expression of Ifi202b (interferon activated gene 202b), a member of the Activity-regulated Inhibitor of Death (AID) gene family that contributes to mitochondrial resistance to cellular stress. Ifi202b has a role in sex-specific inflammatory diseases, which is consistent with our observation. Female KO microglia had enhanced Ifi202b expression, along with the secretion of Ifi202b associated cytokines, including interleukin-6. Treatment of wild-type female microglia with a JAM-A function blocking antibody demonstrated an increase in Ifi202b levels, confirming direct regulation of Ifi202b expression by neutralizing JAM-A. While cell intrinsic, sex-specific differences have been reported in GBM, our findings demonstrate that differences in the GBM tumor microenvironment also drive sexually dimorphic tumor growth.

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Rozzo, Stephen J., John D. Allard, Divaker Choubey, Timothy J. Vyse, Shozo Izui, Gary Peltz, and Brian L. Kotzin. "Evidence for an Interferon-Inducible Gene, Ifi202, in the Susceptibility to Systemic Lupus." Immunity 15, no. 3 (September 2001): 435–43. http://dx.doi.org/10.1016/s1074-7613(01)00196-0.

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Skov, Vibe, Caroline Riley, Mads Thomassen, Lasse Kjær, Thomas Stauffer Larsen, Ole Weis Bjerrum, Torben A. Kruse, and Hans Carl Hasselbalch. "The Impact of Interferon on Interferon-Related Genes in Polycythemia Vera and Allied Neoplasms." Blood 132, Supplement 1 (November 29, 2018): 4328. http://dx.doi.org/10.1182/blood-2018-99-110602.

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Abstract Introduction: Using whole blood transcriptional profiling, we have previously shown deregulation of several interferon-stimulated genes (ISG) and deregulation of immune and inflammation genes in MPNs as well. Most lately, we have shown that deregulated HLA-genes are upregulated by interferon-alpha2 (IFN) treatment. Herein, we for the first time describe the landscape of ISGs during treatment with IFN, the aims being to describe if unique ISG transcriptional signatures might be elicited during IFN treatment with potential differences between subgroups. Methods: Eight patients with ET, 21 patients with PV, and 4 patients with PMF participated in the study. All patients received treatment with IFN, in the large majority in a dosage ranging from 45-90 ug x 1 sc/week. Gene expression microarray analysis of whole blood was performed before and after 3 months of treatment. Total RNA was purified from whole blood, amplified to biotin-labeled RNA, and hybridized to Affymetrix HG-U133 2.0 Plus chips recognizing 54,675 probe sets (38,500 genes). Results: We identified 6261, 10,008, and 2828 probe sets to be significantly differentially expressed in ET, PV, and PMF, respectively, in response to treatment with IFN (pvalue < 0.05). Twenty-one previously identified ISGs were investigated: Six genes involved the response to virus: ISG15, IFI35, IFI44, IFIH1, MX1, and OAS1, 2 transcriptional regulators: IFI16 and SP110, and 13 IFN-inducible genes: ADAR, CXCL10, IFI6, IFI27, IFI30, IFI44L, IFIT1, IFIT2, IFIT3, IFITM1, IFITM2, PSME1, and PYHIN1. Significant upregulation of 20, 21, and 18 ISGs was found in patients with ET, PV, and PMF, respectively. None of the 21 genes was significantly downregulated in any of the patient groups. The 6 genes involved in response to virus and the 2 transcriptional genes were significantly upregulated in all subgroups. In patients with ET all but one gene (CXCL10) of the 13 IFN-inducible genes were significantly upregulated. In patients with PV all 13 IFN-inducible genes were significantly upregulated and in PMF all but three (CXCL10, IFITM2, PUHIN1) IFN-inducible genes were significantly upregulated. No significant differences between subgroups were recorded (data not shown). Discussion and Conclusions: Eighteen genes were significantly upregulated compared to baseline values in all 3 MPN-subgroups. The CXCL10 gene was not significantly regulated in ET and PMF during IFN treatment but significantly upregulated in PV. CXCL10 is involved in the activation of neutrophils. Accordingly, impaired regulation of CXCL10 on exposure to IFN might compromise recruitment and activation of neutrophils. The excessively high expression levels of IFI27 after IFN are intriguing but might be explained by the reported high circulating levels of regulatory T cells (Tregs) after IFN. Thus, Tregs produce TGF-beta which stimulates IFI27. Indeed, TGF-beta was significantly upregulated in ET and PV but not in PMF, likely due to the low number of PMF patients. Surprisingly, we did not find any differences in ISG responses between MPNs. Indeed, taken into account that the MPNs depict a biological continuum from the early cancer stages (ET/PV) to the advanced "metastatic" myelofibrosis stage, different ISG signatures between the subtypes might be anticipated for several reasons. First, such differentiated signatures might exist merely reflecting the heterogeneity between subgroups in regard to "tumor burden". Second, differences in frequencies and functionality of immune cells between the subgroups as shown in most recent studies might impact the ISG signatures. Third, chronic inflammation, considered the driving force for clonal evolution in MPNs, has been shown to compromise cell responses to IFN, implying that PMF patients with the most pronounced inflammatory state might exhibit blunted ISG responses. However, the low number of PMF patients may account for the non-significant difference between ET/PV and PMF. In conclusion, except for 4 genes (CXCL10, IFITM1, IFITM2, and PYHIN1), our study has shown the ISGs to be significantly upregulated in all MPN- subtypes after 3 months of exposure to IFN. The reasons for the absence of upregulation of the above 4 genes are unknown but chronic inflammation and immune deregulation might be influential. Further transcriptional studies of ISGs during IFN treatment in larger study populations and with longer exposure times are needed to address these issues. Table. Table. Disclosures Hasselbalch: Novartis: Research Funding.

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Storek, Kelly M., Nina A. Gertsvolf, Maikke B. Ohlson, and Denise M. Monack. "cGAS and Ifi204 Cooperate To Produce Type I IFNs in Response to Francisella Infection." Journal of Immunology 194, no. 7 (February 20, 2015): 3236–45. http://dx.doi.org/10.4049/jimmunol.1402764.

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Zhang, Jian-Gang, Wei Chen, Cheng-Kai Zhou, Ke Ma, Zhen-Zhen Liu, Yu Gao, Xiao-Qi Lin, and Yong-Jun Yang. "IFI204 protects host defense against Staphylococcus aureus-induced pneumonia by promoting extracellular traps formation." Experimental Cell Research 422, no. 1 (January 2023): 113415. http://dx.doi.org/10.1016/j.yexcr.2022.113415.

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Kim, Hyungsoo, Heejung Kim, Yongmei Feng, Yan Li, Hironari Tamiya, Stefania Tocci, and Ze’ev A. Ronai. "PRMT5 control of cGAS/STING and NLRC5 pathways defines melanoma response to antitumor immunity." Science Translational Medicine 12, no. 551 (July 8, 2020): eaaz5683. http://dx.doi.org/10.1126/scitranslmed.aaz5683.

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Protein arginine methyltransferase 5 (PRMT5) controls diverse cellular processes and is implicated in cancer development and progression. Here, we report an inverse correlation between PRMT5 function and antitumor immunity. PRMT5 expression was associated with an antitumor immune gene signature in human melanoma tissue. Reducing PRMT5 activity antagonized melanoma growth in immunocompetent but not immunocompromised mice. PRMT5 methylation of IFI16 [interferon-γ (IFN-γ)–inducible protein 16] or its murine homolog IFI204, which are components of the cGAS/STING (stimulator of IFN genes) pathway, attenuated cytosolic DNA–induced IFN and chemokine expression in melanoma cells. PRMT5 also inhibited transcription of the gene encoding NLRC5 (nucleotide-binding oligomerization domain-like receptor family caspase recruitment domain containing 5), a protein that promotes the expression of genes implicated in major histocompatibility complex class I (MHCI) antigen presentation. PRMT5 knockdown augmented IFN and chemokine production and increased MHCI abundance in melanoma. Increased expression of IFI204 and NLRC5 was associated with decreased melanoma growth in murine models, and increased expression of IFI16 and NLRC5 correlated with prolonged survival of patients with melanoma. Combination of pharmacological (GSK3326595) or genetic (shRNA) inhibition of PRMT5 with immune checkpoint therapy limited growth of murine melanoma tumors (B16F10 and YUMM1.7) and enhanced therapeutic efficacy, compared with the effect of either treatment alone. Overall, our findings provide a rationale to test PRMT5 inhibitors in immunotherapy-based clinical trials as a means to enhance an antitumor immune response.

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Heller, Loree, Katarina Znida, Masa Bosnjak, Amanda Sales Conniff, Tanja Jesenko, Bostjan Markelc, Jared Tur, Nina Semenova, and Maja Cemazar. "Comparison of DNA sensing by non-immune cells and tissues." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 164.06. http://dx.doi.org/10.4049/jimmunol.208.supp.164.06.

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Abstract Pattern recognition receptors (PRRs) are nearly ubiquitous in both immune and non-immune mammalian cells. PRRs detect pathogen invasion as well as internal damage, inducing the secretion of pro-inflammatory molecules and cell death. Members of the PRR subset that detect intracellular DNA are termed DNA sensors. We examined DNA sensing in non-immune cells and their equivalent tissues using electroporation. This physical delivery method mitigates the need for viral or chemical agents that could confound the source of PRR activation. We used RT-qPCR and/or RNA-Seq to quantify mRNAs encoding DNA sensors and their signaling pathways and western blots, ELISAs and bead arrays to quantify related proteins. Several tumor cell types and non-tumor cells, including keratinocytes, fibroblasts, and myoblasts, expressed different DNA sensors at baseline and responded to backbone plasmid DNA delivery with individual DNA sensor signatures. Some similarities were observed among all these cell types, including upregulation of the DNA sensors ZBP1, DDX60, and Ifi204, the mouse analog of human Ifi16. Each cell type secreted a range of pro-inflammatory molecules including Type I interferon. DNA electroporation to B16-F10 melanomas, skin, and skeletal muscle induced unique cytokine and chemokine signatures, paralleling cellular signatures. ZBP1, DDX60, and Ifi204 were upregulated in skin and muscle; however, no significant regulation was observed in tumors. In muscle particularly, this may be due to the homogeneity of the tissue; tumors are inherently heterogeneous, producing an assortment of individual cellular responses. Supported by NIH grant R01CA196796.

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Wattanapitayakula, Suvara K., Linda Chularojmontri, and Monika Schäfer-Korting. "Ultraviolet B irradiation-induced keratinocyte senescence and impaired development of 3D epidermal reconstruct." Acta Pharmaceutica 71, no. 2 (November 4, 2020): 293–303. http://dx.doi.org/10.2478/acph-2021-0011.

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Abstract Ultraviolet B (UVB) induces morphological and functional changes of the skin. This study investigated the effect of UVB on keratinocyte senescence and the development of reconstructed human epidermis (RHE). Primary normal human keratinocytes (NHK) from juvenile foreskin were irradiated with UVB (30 mJ cm−2) and these effects were compared to NHK that underwent senescence in the late passage. UVB enhanced the accumulation of reactive oxygen species (ROS) and halted cell replication as detected by BrdU cell proliferation assay. The senescence phenotype was evaluated by beta-galactosidase (β-gal) staining and qPCR of genes related to senescent regulation, i.e. p16INK4a, cyclin D2, and IFI27. Senescence induced by high dose UVB resulted in morphological changes, enhanced β-gal activity, elevated cellular ROS levels and reduced DNA synthesis. qPCR revealed differential expression of the genes regulated senescence. p16INK4a expression was significantly increased in NHK exposed to UVB whereas enhanced IFI27 expression was observed only in cultural senescence. The levels of cyclin D2 expression were not significantly altered either by UVB or long culturing conditions. UVB significantly induced the aging phenotype in keratinocytes and impaired epidermal development. RHE generated from UVB-irradiated keratinocytes showed a thinner cross-sectional structure and the majority of keratinocytes in the lower epidermis were degenerated. The 3D epidermis model is useful in studying the skin aging process.

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Cao, Liu, Yanxi Ji, Lanyi Zeng, Qianyun Liu, Zhen Zhang, Shuting Guo, Xiaolong Guo, et al. "P200 family protein IFI204 negatively regulates type I interferon responses by targeting IRF7 in nucleus." PLOS Pathogens 15, no. 10 (October 11, 2019): e1008079. http://dx.doi.org/10.1371/journal.ppat.1008079.

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De Andrea, Marco, Monica Ravotto, Emanuela Noris, Guo-Guang Ying, Daniela Gioia, Barbara Azzimonti, Marisa Gariglio, and Santo Landolfo. "The interferon-inducible gene, Ifi204, acquires malignant transformation capability upon mutation at the Rb-binding sites." FEBS Letters 515, no. 1-3 (March 4, 2002): 51–57. http://dx.doi.org/10.1016/s0014-5793(02)02431-6.

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Suomela, Sari, Li Cao, Anne Bowcock, and Ulpu Saarialho-Kere. "Interferon α-Inducible Protein 27 (IFI27) is Upregulated in Psoriatic Skin and Certain Epithelial Cancers." Journal of Investigative Dermatology 122, no. 3 (March 2004): 717–21. http://dx.doi.org/10.1111/j.0022-202x.2004.22322.x.

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Skov, Vibe, Thomas Stauffer Larsen, Mads Thomassen, Caroline Hasselbalch Riley, Morten K. Jensen, Ole Weis Bjerrum, Torben A. Kruse, and Hans Carl Hasselbalch. "Whole-blood transcriptional profiling of interferon-inducible genes identifies highly upregulated IFI27 in primary myelofibrosis." European Journal of Haematology 87, no. 1 (June 22, 2011): 54–60. http://dx.doi.org/10.1111/j.1600-0609.2011.01618.x.

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Min, Zhu, Zhu Ye, Li Gang, Du Boyu, and Xi Xueyan. "IFI27 as a potential indicator for severe Enterovirus 71-infected hand foot and mouth disease." Virus Research 289 (November 2020): 198149. http://dx.doi.org/10.1016/j.virusres.2020.198149.

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Stadion, Mandy, Kristin Schwerbel, Antonia Graja, Christian Baumeier, Maria Rödiger, Wenke Jonas, Christian Wolfrum, et al. "Increased Ifi202b/IFI16 expression stimulates adipogenesis in mice and humans." Diabetologia 61, no. 5 (February 24, 2018): 1167–79. http://dx.doi.org/10.1007/s00125-018-4571-9.

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Zimmerman, Mary, Dafeng Yang, Xiaolin Hu, Feiyan Liu, Nagendra Singh, Darren Browning, Vadivel Ganapathy, et al. "IFN-γ Upregulates Survivin and Ifi202 Expression to Induce Survival and Proliferation of Tumor-Specific T Cells." PLoS ONE 5, no. 11 (November 22, 2010): e14076. http://dx.doi.org/10.1371/journal.pone.0014076.

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Deschamps, Stéphane, Jeffrey Meyer, Gouri Chatterjee, Hong Wang, Peter Lengyel, and Bruce A. Roe. "The mouse Ifi200 gene cluster: genomic sequence, analysis, and comparison with the human HIN-200 gene cluster☆." Genomics 82, no. 1 (July 2003): 34–46. http://dx.doi.org/10.1016/s0888-7543(03)00092-2.

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Tian, Maobo, Fang Song, Xiangshu Long, Jing Huang, and Qiang Wu. "GW26-e3869 Effects of ifi204 Gene Expression on Apoptosis and Migration of Vascular Adventitial Fibroblast In Rat." Journal of the American College of Cardiology 66, no. 16 (October 2015): C24—C25. http://dx.doi.org/10.1016/j.jacc.2015.06.1121.

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Adam, Benjamin A., Naoka Murakami, Graeme Reid, Katie Du, Ruqaya Jasim, Christie L. Boils, Lihong Bu, et al. "Gene Expression Profiling in Kidney Transplants with Immune Checkpoint Inhibitor–Associated Adverse Events." Clinical Journal of the American Society of Nephrology 16, no. 9 (July 9, 2021): 1376–86. http://dx.doi.org/10.2215/cjn.00920121.

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Background and objectivesImmune checkpoint inhibitors are increasingly used to treat various malignancies, but their application in patients with kidney transplants is complicated by high allograft rejection rates. Immune checkpoint inhibitor–associated rejection is a novel, poorly understood entity demonstrating overlapping histopathologic features with immune checkpoint inhibitor–associated acute interstitial nephritis, which poses a challenge for diagnosis and clinical management. We sought to improve the understanding of these entities through biopsy-based gene expression analysis.Design, setting, participants, & measurementsNanoString was used to measure and compare the expression of 725 immune-related genes in 75 archival kidney biopsies, including a 25-sample discovery cohort comprising pure T cell–mediated rejection and immune checkpoint inhibitor–associated acute interstitial nephritis and an independent 50-sample validation cohort comprising immune checkpoint inhibitor–associated acute interstitial nephritis, immune checkpoint inhibitor–associated T cell–mediated rejection, immune checkpoint inhibitor–associated crescentic GN, drug-induced acute interstitial nephritis, BK virus nephropathy, and normal biopsies.ResultsSignificant molecular overlap was observed between immune checkpoint inhibitor–associated acute interstitial nephritis and T cell–mediated rejection. Nevertheless, IFI27, an IFN-α–induced transcript, was identified and validated as a novel biomarker for differentiating immune checkpoint inhibitor–associated T cell–mediated rejection from immune checkpoint inhibitor–associated acute interstitial nephritis (validation cohort: P<0.001, area under the receiver operating characteristic curve =100%, accuracy =86%). Principal component analysis revealed heterogeneity in inflammatory gene expression patterns within sample groups; however, immune checkpoint inhibitor–associated T cell–mediated rejection and immune checkpoint inhibitor–associated acute interstitial nephritis both demonstrated relatively more molecular overlap with drug-induced acute interstitial nephritis than T cell–mediated rejection, suggesting potential dominance of hypersensitivity mechanisms in these entities.ConclusionsThese results indicate that, although there is significant molecular similarity between immune checkpoint inhibitor–associated rejection and acute interstitial nephritis, biopsy-based measurement of IFI27 gene expression represents a potential biomarker for differentiating these entities.

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Singh, Ram P., Ravi Dinesh, Antonio La Cava, and Bevra H. Hahn. "Tolerization of BWF1 lupus mice with pConsensus peptide results in a distinct gene signature in WBC, CD4+ and CD8+T cells: Role of Foxp3 and IFI202b in suppression of SLE (50.22)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 50.22. http://dx.doi.org/10.4049/jimmunol.182.supp.50.22.

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Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease associated with autoantibodies, including IgG anti-DNA and immune complexes. Following tolerization with an artificial peptide (pCONSENSUS, pCons) that is based on anti-DNA IgG sequences containing MHC class I and class II T cell determinants, NZB/NZW F1 female (BWF1) mice develop CD4+CD25+ regulatory T cells and CD8+ Foxp3+ inhibitory T cells, both of which suppress anti-DNA Ig production. In this study, we analyzed 45,000 murine genes using Affymetrix Gene Chip 430, 2.0 arrays, in a comparison of total white blood cells (WBC), CD4, and CD8 spleen cell subsets from tolerized vs. non-tolerized mice. Results showed 448, 174 and 60 genes that were differentially expressed by at least two-fold in the two groups of mice. From the CD8+T cell arrays, we confirmed up regulation of several genes in cells from tolerized mice using real-time PCR. Increased expression (more than two-fold) in the CD8+Tcells from tolerized mice was repeatedly found for six genes: IFI202B, Bcl2, Foxp3, Trp-53, CCR7 and IFNar1. Silencing with siRNA of IFI202b and bcl2 abrogated the suppressive capacity of the tolerized CD8+T cells. In contrast, silencing of IFNar1 and CCR7 had no effect on the ability of the CD8+T cells to suppress autoantibody production. Further silencing of combination of multiple genes affected other genes in addition to silenced gene/genes in tolerized CD8+T cells. These data indicate the roles of IFI202b, Foxp3, bcl2, and further demonstrate that silencing of one gene or combinations may affect other genes and or their functions.

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Choubey, D., R. Panchanathan, and H. Liu. "Interferon-inducible Ifi202b gene in (NZB × NZW)F1 lupus-prone mice." Genes & Immunity 12, no. 6 (July 7, 2011): 495. http://dx.doi.org/10.1038/gene.2011.47.

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Xin, Hong, Sanjay D’Souza, Trine N. Jørgensen, Andrew T. Vaughan, Peter Lengyel, Brian L. Kotzin, and Divaker Choubey. "Increased Expression of Ifi202, an IFN-Activatable Gene, in B6.Nba2 Lupus Susceptible Mice Inhibits p53-Mediated Apoptosis." Journal of Immunology 176, no. 10 (May 2, 2006): 5863–70. http://dx.doi.org/10.4049/jimmunol.176.10.5863.

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Xin, Hong, Rocky Pramanik, and Divaker Choubey. "Retinoblastoma (Rb) protein upregulates expression of the Ifi202 gene encoding an interferon-inducible negative regulator of cell growth." Oncogene 22, no. 31 (July 2003): 4775–85. http://dx.doi.org/10.1038/sj.onc.1206780.

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Shaath, Hibah, Radhakrishnan Vishnubalaji, Eyad Elkord, and Nehad M. Alajez. "Single-Cell Transcriptome Analysis Highlights a Role for Neutrophils and Inflammatory Macrophages in the Pathogenesis of Severe COVID-19." Cells 9, no. 11 (October 29, 2020): 2374. http://dx.doi.org/10.3390/cells9112374.

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Cumulative data link cytokine storms with coronavirus disease 2019 (COVID-19) severity. The precise identification of immune cell subsets in bronchoalveolar lavage (BAL) and their correlation with COVID-19 disease severity are currently being unraveled. Herein, we employed iterative clustering and guide-gene selection 2 (ICGS2) as well as uniform manifold approximation and projection (UMAP) dimensionality reduction computational algorithms to decipher the complex immune and cellular composition of BAL, using publicly available datasets from a total of 68,873 single cells derived from two healthy subjects, three patients with mild COVID-19, and five patients with severe COVID-19. Our analysis revealed the presence of neutrophils and macrophage cluster-1 as a hallmark of severe COVID-19. Among the identified gene signatures, IFITM2, IFITM1, H3F3B, SAT1, and S100A8 gene signatures were highly associated with neutrophils, while CCL8, CCL3, CCL2, KLF6, and SPP1 were associated with macrophage cluster-1 in severe-COVID-19 patients. Interestingly, although macrophages were also present in healthy subjects and patients with mild COVID-19, they had different gene signatures, indicative of interstitial and cluster-0 macrophage (i.e., FABP4, APOC1, APOE, C1QB, and NURP1). Additionally, MALAT1, NEAT1, and SNGH25 were downregulated in patients with mild and severe COVID-19. Interferon signaling, FCγ receptor-mediated phagocytosis, IL17, and Tec kinase canonical pathways were enriched in patients with severe COVID-19, while PD-1 and PDL-1 pathways were suppressed. A number of upstream regulators (IFNG, PRL, TLR7, PRL, TGM2, TLR9, IL1B, TNF, NFkB, IL1A, STAT3, CCL5, and others) were also enriched in BAL cells from severe COVID-19-affected patients compared to those from patients with mild COVID-19. Further analyses revealed genes associated with the inflammatory response and chemotaxis of myeloid cells, phagocytes, and granulocytes, among the top activated functional categories in BAL from severe COVID-19-affected patients. Transcriptome data from another cohort of COVID-19-derived peripheral blood mononuclear cells (PBMCs) revealed the presence of several genes common to those found in BAL from patients with severe and mild COVID-19 (IFI27, IFITM3, IFI6, IFIT3, MX1, IFIT1, OASL, IFI30, OAS1) or to those seen only in BAL from severe-COVID-19 patients (S100A8, IFI44, IFI44L, CXCL8, CCR1, PLSCR1, EPSTI1, FPR1, OAS2, OAS3, IL1RN, TYMP, BCL2A1). Taken together, our data reveal the presence of neutrophils and macrophage cluster-1 as the main immune cell subsets associated with severe COVID-19 and identify their inflammatory and chemotactic gene signatures, also partially reflected systemically in the circulation, for possible diagnostic and therapeutic interventions.

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De Andrea, Marco, Claudia Zannetti, Emanuela Noris, Marisa Gariglio, Barbara Azzimonti, and Santo Landolfo. "The Mouse Interferon-Inducible Gene Ifi204 Product Interacts with the Tpr Protein, a Component of the Nuclear Pore Complex." Journal of Interferon & Cytokine Research 22, no. 11 (November 2002): 1113–21. http://dx.doi.org/10.1089/10799900260442539.

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Tian, Cheng, Xiaoyun Liu, Xiaodong Zhu, Yanhong Cao, Nan Deng, Karen A. Hasty, John M. Stuart, Weikuan Gu, and Yan Jiao. "Ifi204 as the most favored candidate gene that regulates susceptibility to spontaneous arthritis in mice deficient in IL-1ra." Gene Reports 12 (September 2018): 21–29. http://dx.doi.org/10.1016/j.genrep.2018.05.006.

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Huang, Shu, Jinglin Zhao, Jianxin Song, Yanqiong Li, Rongxia Zuo, Yalian Sa, Zhihui Ma, and Hongmei OuYang. "Interferon alpha-inducible protein 27 (IFI27) is a prognostic marker for pancreatic cancer based on comprehensive bioinformatics analysis." Bioengineered 12, no. 1 (January 1, 2021): 8515–28. http://dx.doi.org/10.1080/21655979.2021.1985858.

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Cheriyath, Venugopalan, Douglas W. Leaman, and Ernest C. Borden. "Emerging Roles of FAM14 Family Members (G1P3/ISG 6–16 and ISG12/IFI27) in Innate Immunity and Cancer." Journal of Interferon & Cytokine Research 31, no. 1 (January 2011): 173–81. http://dx.doi.org/10.1089/jir.2010.0105.

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Nagasawa, Yasuyuki, Daisuke Okuzaki, Eri Muso, Ryohei Yamamoto, Maki Shinzawa, Yukako Iwasaki, Hirotsugu Iwatani, Takeshi Nakanishi, Yoshitaka Isaka, and Hiroshi Nojima. "IFI27 Is a Useful Genetic Marker for Diagnosis of Immunoglobulin A Nephropathy and Membranous Nephropathy Using Peripheral Blood." PLOS ONE 11, no. 4 (April 21, 2016): e0153252. http://dx.doi.org/10.1371/journal.pone.0153252.

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Cecchi, I., M. Radin, A. Barinotti, S. G. Foddai, E. Rubini, A. Suárez, D. Roccatello, S. Sciascia, and J. Rodríguez-Carrio. "POS0092 HETEROGENEITY OF THE TYPE I INTERFERON SIGNATURE AMONG ANTIPHOSPHOLIPID SYNDROME PATIENTS: A CLUSTER AND CORRESPONDENCE ANALYSIS APPROACH." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 267.2–268. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4631.

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BackgroundType I Interferons (IFN) are central players in the pathogenesis, disease activity and evolution of several autoimmune conditions. To date, a limited number of evidences is available on the specific role of IFN activation in antiphospholipid antibodies (aPL) positive patients, including aPL carriers, primary antiphospholipid syndrome (PAPS) and those APS subjects who presented with an associated autoimmune disease (secondary APS, SAPS), such as systemic lupus erythematosus (SLE).ObjectivesThe aim of this study was to evaluate the differential expression of IFN stimulated genes (ISG) among different subsets of aPL positive subjects and SLE patients.MethodsFor the purpose of the study, a total of 112 patients attending the San Giovanni Bosco Hospital (Turin, Italy) were enrolled, including 31 PAPS, 25 SAPS, 27 SLE patients without aPL, 29 aPL carriers (mean age 48.3±13.3 years, 76% female)1,2. Nineteen subjects were also recruited as healthy controls (HCs). Complete demographic, clinical, and laboratory data were collected at the time of the inclusion. Gene expression was evaluated by RT-PCR in whole blood for the following genes: IFI6, IFI44, IFI44L, MX1,IFI27, OAS1 and RSAD2. Normalized gene expression levels (Z-scores) were averaged into a global IFN signature (IFN score). Differences were measured by Kruskal-Wallis tests and associations among genes were studied by cluster and correspondence analyses. Correlations among genes were plotted by network analyses.ResultsAn overall activation of ISG was noted across APS subsets, but certain differences were noted among genes. Whereas some ISG were already upregulated in the aPL positive group compared to HC (IFI44, IFI44L, MX1, IFI27, OAS1 and RSAD2, all p<0.050), other ISG were only in increased SLE (IFI6), MX1 differed between SLE and SAPS, and IFI27 and OAS1 showed differences between PAPS and SAPS. The composite IFN score revealed quantitative differences in the IFN pathway activation across APS subsets, being elevated in aPL carriers/PAPS groups compared to HCs (both p<0.050) and increasing in SAPS (p<0.010) and SLE (p<0.001) groups. Network analyses (Figure 1A) revealed qualitative differences in the gene-gene correlation networks: (i) weaker structures were found in HCs and aPL carriers, compared to stronger and higher-degree networks in SAPS and SLE groups; and (ii) the influence of each node was different across groups. Unsupervised cluster analysis identified 3 clusters (I to III) based on ISG patterns (Figure 1B). Clusters usage differed among APS subsets, thus correlating clinical status (Figure 1C). Distinct groups of ISG positively correlate to aPS/PT IgG titre in aPL carriers and PAPS groups (all rho>0.500), whereas no associations were retrieved in SAPS or SLE. No associations with previous thrombotic events were observed in any subset, although IFN composite score and several ISG correlate with the number of thrombotic recurrences under anticoagulation (all rho>0.400). No associations with GAPSS were observed.Figure 1.ConclusionAn overall IFN pathway activation has been observed in aPL positive patients and across all APS subsets. Qualitative and quantitative differences across the APS spectrum can be identified, leading to the identification of distinct IFN signatures with different clinical value.References[1]Miyakis S, et al. J Thromb Haemost (2006). 2. Aringer M, et al. Arthritis Rheumatol (2019).Disclosure of InterestsNone declared

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Panchanathan, Ravichandran, Hui Shen, Melanie Gubbels Bupp, Karen A. Gould, and Divaker Choubey. "Female and Male Sex Hormones Differentially Regulate Expression of Ifi202, an Interferon-Inducible Lupus Susceptibility Gene within the Nba2 Interval." Journal of Immunology 183, no. 11 (November 4, 2009): 7031–38. http://dx.doi.org/10.4049/jimmunol.0802665.

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Panchanathan, Ravichandran, Xin Duan, Hui Shen, Vijay A. K. Rathinam, Loren D. Erickson, Katherine A. Fitzgerald, and Divaker Choubey. "Aim2 Deficiency Stimulates the Expression of IFN-Inducible Ifi202, a Lupus Susceptibility Murine Gene within the Nba2 Autoimmune Susceptibility Locus." Journal of Immunology 185, no. 12 (November 5, 2010): 7385–93. http://dx.doi.org/10.4049/jimmunol.1002468.

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