Journal articles: 'Interferoni'

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Cavallo, Giorgio, Marisa Gariglio, Saverio Panico, and Santo Landolfo. "Regolazione delľ espressione genicain vivo da parte degli interferoni." Rendiconti Lincei 1, no. 1 (March 1990): 105–9. http://dx.doi.org/10.1007/bf03001755.

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Betterle, Corrado, and Fabio Presotto. "Terapia con interferoni e autoimmunità organo-specifica: quali rischi e come gestire il paziente." L'Endocrinologo 11, no. 5 (October 2010): 198–206. http://dx.doi.org/10.1007/bf03344741.

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Larsen, Thomas Stauffer, Michael Boe Møller, Karin de Stricker, Peter Nørgaard, Jan Samuelsson, Claus Marcher, Ole Weis Bjerrum, Morten T. Andersen, and Hans Carl Hasselbalch. "Minimal Residual Disease and Normalization of the Bone Marrow after Long-Term Treatment with Alpha-Interferon2b in Polycythemia Vera. A Report on Seven Patients in Sustained Complete Hematological Remission with Major Molecular Responses." Blood 112, no. 11 (November 16, 2008): 1744. http://dx.doi.org/10.1182/blood.v112.11.1744.1744.

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Abstract Background : Polycythemia vera (PV) is a clonal myeloproliferative disorder characterized by the presence of the JAK2V617 mutation in virtually all patients. Recently several studies have shown that the JAK2V617F mutational load decreases during treatment with alpha-interferon2 (1–6). Aim: To report on molecular and histomorphological bone marrow responses in seven PV patients with complete molecular remissions during and after long-term treatment with alpha-interferon 2b. Patients: Seven patients treated with alpha-interferon2b for a median of 84 months (range 31–120) are reported. In four of the patients alpha-interferon2b was started at the time of diagnosis and in three patients 9, 36 and 42 months from the time of diagnosis, respectively. Methods: The mutation was determined by allele specific PCR (n=2 only) (7) and quantitative PCR (qPCR) (n=5) (8). In three out of these patients qPCR JAK2V617F was performed on archived bone marrow from diagnosis (2 patients) and on peripheral blood (one patient) prior to treatment with alpha-interferon2b. A complete molecular remission (CMoR) was defined by less than 2 % JAK2 V617F mutated alleles (7). Results: Molecular Responses. All patients obtained a CMoR after a median of 84 months (29–120 months) of treatment with alpha-interferon2b. Subsequently all patients have discontinued alpha-interferon with a follow-up period of median 10 months (range 4–30 months) and sustained complete hematological remission. Furthermore, in three patients molecular responses have recently been updated – April and May 2008 - showing CMoRs in all (1,2 %, 0,9 % 0,1 % mutated alleles, respectively). Bone Marrow Responses. Follow-up bone marrow biopsies were available in five patients. Complete normalization of the bone marrow was seen in three patients after treatment with alpha-interferon2b for 84, 132 and 132 months, respectively. In the bone marrow from the patient being treated with alpha-interferon for 132 months a qPCR JAK2V617 analysis was performed detecting the mutation at a very low level (0,5 % mutated alleles). In two other patients, being treated with alpha-interferon2b for 24 and 120 months, respectively, and having obtained a CmoR in peripheral blood the bone marrow histomorphology showed marked regression of PV-features but in both patients still with focal areas displaying an increased number of morphologically abnormal megakaryocytes. Updated histomorphological and molecular response patterns will be presented. Discussion and Conclusion : Previous studies on the molecular response during alpha-interferon2a treatment have shown that a substantial proportion of patients achieve a significant molecular response after 12 months with a continuous decrease in the JAK2V617F mutation load at 24 and 36 months (1,5,6). This report confirms and extends preliminary data, showing that long-term treatment with alpha-interferon 2b in a subgroup of PV-patients is able to induce complete molecular remissions with normalization of the bone marrow morphology, which may even be sustained after discontinuation of alpha-interferon2b for up to 20 months (5). Prolonged treatment for several years seems necessary to induce such sustained responses, since treatment for only a few months has been reported to be followed by rapid recurrence of clonal hematopoiesis (9). In conclusion, a state of “minimal residual disease” may be achieved in PV by long-term immune therapy using alpha-interferon 2. Our observations call for large prospective clinical studies in which treatment with alpha-interferon is initiated up-front in patients with JAK2-positive PV and allied diseases. These studies should also aim at exploring the minimal dose of alpha-interferon needed to elicit complete molecular responses in order to minimize side effects of the drug and accordingly diminish the high drop-out rates reported in most previous studies.

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Muttar, A. A. "Cloning and gene expression equine leukocyte α-interferon in cells of Escherichia Coli." Al-Qadisiyah Journal of Veterinary Medicine Sciences 12, no. 1 (June 30, 2013): 82. http://dx.doi.org/10.29079/vol12iss1art234.

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Interferon plays role in innate immune responses through upregulation of costimulatory molecules and induction of proinflammatory cytokines. interferons including interferon alpha (IFNA). The present study characterized IFNA cDNA and predicted protein. The interferon’s play a great role in protection from infections, which have been called by microorganisms, and also have powerful antiproliferation and immunomodulation activity. The purposes of study: cloning and expression of horse leukocyte interferon and purification the product protein. The results and discussion : In the result we isolated (DNA) from equine leukocyte in blood, which was used in the quality of the matrix for amplification of α-interferon gene with PCR HELP, and isolation gene α-interferon and transformation in vector puc18 and expression vector PET24b (+) and recombinant plasmid was transformed into E. coli strain BL21( codon plus 440) induction with IPTG. The results showed the protein having the same molecular weight as horse interferon alpha about 5.81 kDa

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Zimring, James C., Stephen Goodbourn, and Margaret K. Offermann. "Human Herpesvirus 8 Encodes an Interferon Regulatory Factor (IRF) Homolog That Represses IRF-1-Mediated Transcription." Journal of Virology 72, no. 1 (January 1, 1998): 701–7. http://dx.doi.org/10.1128/jvi.72.1.701-707.1998.

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ABSTRACT Human herpesvirus 8 (HHV-8) is the probable viral etiologic agent for Kaposi’s sarcoma. The HHV-8 genome encodes viral interferon regulatory factor (vIRF), a gene product that has homology to the IRF family of transcription factors. We demonstrate that vIRF inhibits responses to type I and type II interferons and blocks IRF-1-mediated transcription. vIRF does not compete with IRF-1 for binding to DNA or complex directly with IRF-1. The ability of vIRF to block IRF-1-mediated transcription is independent of the DNA binding domains of both vIRF and IRF-1. These data suggest that vIRF may contribute to viral pathogenesis and cellular transformation by interfering with interferon- and IRF-1-mediated gene expression through a novel mechanism.

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Foley, John F. "Interfering with interferons." Science Signaling 9, no. 415 (February 16, 2016): ec30-ec30. http://dx.doi.org/10.1126/scisignal.aaf4271.

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Wilks, J., and T. Golovkina. "Interfering with interferons." Science 347, no. 6219 (January 15, 2015): 233–34. http://dx.doi.org/10.1126/science.aaa5056.

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Mueller, K. L. "Interfering with Interferons." Science Signaling 6, no. 268 (March 26, 2013): ec75-ec75. http://dx.doi.org/10.1126/scisignal.2004169.

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Simpson, S. "Interfering with Interferon." Science's STKE 2007, no. 376 (February 28, 2007): tw81. http://dx.doi.org/10.1126/stke.3762007tw81.

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Polyak, Stephen J. "Interfering with interferon." Trends in Microbiology 7, no. 10 (October 1999): 401. http://dx.doi.org/10.1016/s0966-842x(99)01592-9.

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Bucci, Mirella. "Interfering with Interferon." Nature Chemical Biology 10, no. 5 (April 17, 2014): 324. http://dx.doi.org/10.1038/nchembio.1511.

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Martz, Lauren. "Interfering with interferon." Science-Business eXchange 6, no. 16 (April 2013): 381. http://dx.doi.org/10.1038/scibx.2013.381.

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Harris, Bethany D., Srilalitha Kuruganti, Ashlesha Deshpande, Paul A. Goepfert, W. Winn Chatham, and Mark R. Walter. "Characterization of Type-I IFN subtype autoantibodies and activity in SLE serum and urine." Lupus 29, no. 9 (July 1, 2020): 1095–105. http://dx.doi.org/10.1177/0961203320935976.

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Background/objective Type-I interferons contribute to pathogenesis in systemic lupus erythematosus, including nephritis. Interferons consist of a family of 16 proteins yet are often characterized in patients without knowledge of the specific interferon subtypes involved. Different interferons may function in the kidneys, and other organs, relative to what is often measured in patient blood. Moreover, antibodies to interferons may potentially modulate systemic or organ-specific interferon activity. The aim of this study was to characterize global interferon activity levels and identify autoantibodies to the 12 interferon α subtypes in patient serum and urine. Methods Interferon activity levels in serum and urine were measured using an interferon bioassay. Anti-interferon and anti-cytokine autoantibodies were measured by ELISA. Serum and urine samples were also characterized for their ability to neutralize the biological activity of exogenously added interferons. Results Serum interferon activity was increased in 62% of systemic lupus erythematosus patient samples, relative to healthy donor controls, whereas binding interferon α autoantibodies to at least one interferon α subtype were found in 68% of the samples evaluated. High Systemic Lupus Erythematosus Disease Activity Index scores were significantly ( p = 0.001) associated with patient samples containing interferon α autoantibodies to three or more interferon α subtypes in their serum. Interferon α autoantibodies that potently block interferon activity were rare (∼5% of samples), but collectively bound to all 12 interferon α subtypes. Urine interferon activity and interferon α autoantibody profiles did not correlate with their serum counterparts, suggesting immune responses in systemic lupus erythematosus kidneys can be distinct from those measured in serum. Analysis of autoantibodies to 15 additional cytokines in serum identified higher frequencies of granulocyte-macrophage colony-stimulating factor and interleukin 17A autoantibodies, suggesting these signaling pathways may potentially contribute, with interferons, to systemic lupus erythematosus pathogenesis. Conclusions The measurement of autoantibodies to multiple interferon subtypes in serum and urine may provide an alternative method for following interferon-mediated systemic lupus erythematosus disease activity. The results suggest autoantibodies might be used for patient monitoring and/or identifying additional cytokine signaling pathways that are functioning in different systemic lupus erythematosus patients.

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MENKES, DAVID B., and JAMES A. MacDONALD. "Interferons, serotonin and neurotoxicity." Psychological Medicine 30, no. 2 (March 2000): 259–68. http://dx.doi.org/10.1017/s0033291799001774.

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Background. Interferons are a class of cytokines profoundly affecting immune function. Several interferons are now synthesized and used clinically, notably for viral diseases and cancer. In addition to their desired immune effects, interferons cause a number of toxicities, including prominent effects on the nervous system.Methods. This literature review focused on the incidence of depression associated with interferon treatment. Possible neurochemical mechanisms and remedial strategies were also considered.Results. Interferon treatment, particularly with the alpha subtype, is unquestionably linked with depression, but the strength of association is uncertain because of erratic ascertainment and pre- treatment co-morbidity. A likely pathogenic mechanism has been described, involving interferon suppression of serotonin synthesis. Controlled treatment trials of interferon-induced depression are not yet available.Conclusions. Neurotoxicity substantially limits the use of interferons. At least some of the risk of depression appears to derive from their anti-serotonergic effects, consistent with the large body of evidence pointing to a general link between serotonin and affective illness. Vigilant detection and aggressive treatment of depression is necessary to optimize interferon treatment of many patients.

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REVEL, MICHEL, ASHER ZILBERSTEIN, ROSE MARIA RUGGIERI, MENACHEM RUBINSTEIN, and LUISA CHEN. "Autocrine Interferons and Interferon-β2." Journal of Interferon Research 7, no. 5 (October 1987): 529–36. http://dx.doi.org/10.1089/jir.1987.7.529.

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Bojic, Ivanko, Ljubisa Dokic, and Svetlana Minic. "Effects of interferons on hepatitis C virus infection." Medical review 59, no. 9-10 (2006): 482–86. http://dx.doi.org/10.2298/mpns0610482b.

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Introduction. The consequences of hepatitis C virus infections (chronic hepatitis, liver cirrhosis and hepatocellular carcinoma) are one of the major problems in clinical medicine. The persistence of infection in spite of high specific antibody titre suggests that the virus has the ability to "escape" the immunological response. Interferon therapy. Interferons are important components of the early host response to infection. They have antiviral, antiproliferative, and immunomodulatory activities. Many viruses have developed the ability to "annul" or alleviate the action of interferon by preventing its synthesis or by interfering with signaling pathways in the cells. During acute infection some of the non-structural proteins of HCV block regulatory factors that are responsible for the synthesis of endogenous infection. Within a cell, interferon induces a number of genes to produce proteins that prevent virus replication. Among them, the most important are RNA-dependent protein kinase and the eukaryotic initiation factor. However, viral proteins, especially viral envelope proteins and nonstructural protein 5A, prevent their phosphorylation and activation which enhance virus replication. These are the facts that have to be considered when using IFN in chronic hepatitis C patients. .

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Chang, Xiaobo, Xibao Shi, Xiaozhuan Zhang, Li Wang, Xuewu Li, Aiping Wang, Ruiguang Deng, Enmin Zhou, and Gaiping Zhang. "IFI16 Inhibits Porcine Reproductive and Respiratory Syndrome Virus 2 Replication in a MAVS-Dependent Manner in MARC-145 Cells." Viruses 11, no. 12 (December 16, 2019): 1160. http://dx.doi.org/10.3390/v11121160.

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Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded positive-sense RNA virus, and the current strategies for controlling PRRSV are limited. Interferon gamma-inducible protein 16 (IFI16) has been reported to have a broader role in the regulation of the type I interferons (IFNs) response to RNA and DNA viruses. However, the function of IFI16 in PRRSV infection is unclear. Here, we revealed that IFI16 acts as a novel antiviral protein against PRRSV-2. IFI16 could be induced by interferon-beta (IFN-β). Overexpression of IFI16 could significantly suppress PRRSV-2 replication, and silencing the expression of endogenous IFI16 by small interfering RNAs led to the promotion of PRRSV-2 replication in MARC-145 cells. Additionally, IFI16 could promote mitochondrial antiviral signaling protein (MAVS)-mediated production of type I interferon and interact with MAVS. More importantly, IFI16 exerted anti-PRRSV effects in a MAVS-dependent manner. In conclusion, our data demonstrated that IFI16 has an inhibitory effect on PRRSV-2, and these findings contribute to understanding the role of cellular proteins in regulating PRRSV replication and may have implications for the future antiviral strategies.

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Barinaga, M. "Immunology. Interfering with interferon." Science 259, no. 5102 (March 19, 1993): 1693–94. http://dx.doi.org/10.1126/science.8456294.

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Smith, Geoffrey L., Julian A. Symons, and Antonio Alcamı́. "Poxviruses: Interfering with Interferon." Seminars in Virology 8, no. 5 (April 1998): 409–18. http://dx.doi.org/10.1006/smvy.1997.0145.

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Sozaeva, L. S. "The new immunological methods for diagnostics of type 1 autoimmune polyendocrine syndrome." Problems of Endocrinology 61, no. 3 (June 15, 2015): 43–46. http://dx.doi.org/10.14341/probl201561343-46.

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Type 1 autoimmune polyglandular syndrome (type 1APS) is a rare genetic disease resulting from mutations in the AIRE gene. Diagnostics of this pathology is based not only on the results of genetic studies but also on the measurement of the level of antibodies against type 1 interferons, such as interferon-ω and interferon-α2. The present review of the literature is focused on type 1 interferons, anti-interferon antibodies, and pathophysiological characteristics of the processes induced by these antibodies.

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de Lemos, Livia Pires, Augusto Guerra, Ramon Pereira, Rosangela Gomes, Isabella Godói, Isabela Diniz, Ivan Zimmermann, et al. "OP40 First Case Of Disinvestment Using Real-World Evidence In Brazil." International Journal of Technology Assessment in Health Care 33, S1 (2017): 18–19. http://dx.doi.org/10.1017/s0266462317001349.

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INTRODUCTION:Beta-interferons are used as first-line therapy for relapsing-remitting multiple sclerosis in Brazil. In order to evaluate the possible inferiority of one of the beta-interferons available and support a guideline update, we conducted an eleven-year (January 2000 to December 2010) nationwide real-world performance assessment using the Unified Health System (SUS) databases.METHODS:We assessed whether patients using subcutaneous beta-interferon switched treatment, relapsed or died (composite event) earlier than patients using intramuscular beta-interferons. Patients without a dispensing registry longer than three months were censored. We used the Kaplan-Meier method to estimate the cumulative probability of persistence on initial treatment, and compared groups with the Log-rank test. The influence of the drug on the occurrence of event was assessed with Cox proportional hazards analysis.RESULTS:The number of patients included was 12,154, and the majority started treatment with subcutaneous beta-interferon-1a (45.7 percent), followed by subcutaneous beta-interferon-1b (27.7 percent) and by intramuscular beta-interferon (26.6 percent). Women represented 73.1 percent and the mean age was 38.93±11.34 years old. The group of patients who used intramuscular beta-interferon switched treatment, relapsed or died earlier (median 47 months; 95 percent Confidence Interval, CI 44–52) than patients using the subcutaneous beta-interferons, (69 months (95 percent CI 64–76) for beta- interferon 1a and 73 (95 percent CI 66–84) months for beta-interferon 1b) (p< .0001 for both comparisons). Accordingly, the use of intramuscular beta-interferon was associated with a higher probability of event (Hazard ratio, HR 1.38; 95 percent CI 1.29-1.48), while the use of the other beta-interferons had a protective effect (1a: HR .86; 95 percent CI .81-.92; 1b: HR .89; 95 percent CI .83-.95).CONCLUSIONS:The inferiority of intramuscular beta-interferon found in the real-world corroborates findings from head-to-head studies and systematic reviews conducted by Cochrane and the National Commission for Technology Incorporation in SUS (CONITEC/Brazil). This result led to disinvestment in intramuscular beta-interferon and was the first case of clinical guideline update using real-world evidence in Brazil.

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Pilna, Hana, Vera Hajkova, Jarmila Knitlova, Jana Liskova, Jana Elsterova, and Zora Melkova. "Vaccinia Virus Expressing Interferon Regulatory Factor 3 Induces Higher Protective Immune Responses against Lethal Poxvirus Challenge in Atopic Organism." Viruses 13, no. 10 (October 3, 2021): 1986. http://dx.doi.org/10.3390/v13101986.

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Vaccinia virus (VACV) is an enveloped DNA virus from the Orthopoxvirus family, various strains of which were used in the successful eradication campaign against smallpox. Both original and newer VACV-based replicating vaccines reveal a risk of serious complications in atopic individuals. VACV encodes various factors interfering with host immune responses at multiple levels. In atopic skin, the production of type I interferon is compromised, while VACV specifically inhibits the phosphorylation of the Interferon Regulatory Factor 3 (IRF-3) and expression of interferons. To overcome this block, we generated a recombinant VACV-expressing murine IRF-3 (WR-IRF3) and characterized its effects on virus growth, cytokine expression and apoptosis in tissue cultures and in spontaneously atopic Nc/Nga and control Balb/c mice. Further, we explored the induction of protective immune responses against a lethal dose of wild-type WR, the surrogate of smallpox. We demonstrate that the overexpression of IRF-3 by WR-IRF3 increases the expression of type I interferon, modulates the expression of several cytokines and induces superior protective immune responses against a lethal poxvirus challenge in both Nc/Nga and Balb/c mice. Additionally, the results may be informative for design of other virus-based vaccines or for therapy of different viral infections.

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Gizinger, O. A. "Interferons and interferon therapy. Literature review." Terapevt (General Physician), no. 7 (May 19, 2021): 46–59. http://dx.doi.org/10.33920/med-12-2107-07.

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The article describes the types and biological characteristics of interferons, which are an integral part of the antiviral defense of the body. The possibilities of using interferons, interferon inducers in the complex treatment of acute respiratory viral infections are shown. The validity and possible risks of using interferon preparations for the treatment and prevention of acute respiratory viral infections are analyzed, taking into account information about their mechanisms of action.

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Nason-Burchenal, K., D. Gandini, M. Botto, J. Allopenna, JR Seale, NC Cross, JM Goldman, E. Dmitrovsky, and PP Pandolfi. "Interferon augments PML and PML/RAR alpha expression in normal myeloid and acute promyelocytic cells and cooperates with all-trans retinoic acid to induce maturation of a retinoid-resistant promyelocytic cell line." Blood 88, no. 10 (November 15, 1996): 3926–36. http://dx.doi.org/10.1182/blood.v88.10.3926.bloodjournal88103926.

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The PML gene is fused to the retinoic acid receptor alpha gene (RAR alpha) in the acute promyelocytic leukemia (APL) 15; 17 translocation. PML is expressed in diverse tissues and cell lines and localized in the nucleus with a typical speckled pattern. In the bone marrow, it is preferentially expressed in myeloid cells. PML appears to be transcriptionally regulated by class I and II interferons, which raises the possibility that interferons modulate the function and growth and differentiation potential of normal myeloid cells and precursors by activating PML-dependent pathways. Similarly, interferons could act on APL cells, alone or in combination with all-trans retinoic acid (RA), especially if the PML/RAR alpha fusion transcript that results from the t(15; 17) is induced by interferon. We report here that PML is expressed at low levels or not expressed in normal circulating human monocytes, lymphocytes, and polymorphonucleate cells, but is markedly induced by interferon; that PML and PML/RAR alpha expression is augmented by interferon in the NB4 APL cell line, which carries the t(15; 17), and in APL blasts from patients; that interferon inhibits growth and survival of NB4 APL cells in cooperation with RA; that interferons alone have minimal maturation effect on NB4 cells; and, finally, that interferon gamma, but not alpha or beta, induces maturation and growth suppression of NB4 cells with de novo retinoid resistance, and partially restores RA response.

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Puoti, Massimo, Sergio Babudieri, Giovanni Rezza, Pierluigi Viale, Maria Giulia Antonini, Ivana Maida, Stefania Rossi, et al. "Use of Pegylated Interferons is Associated with An Increased Incidence of Infections during Combination Treatment of Chronic Hepatitis C: A Side Effect of Pegylation?" Antiviral Therapy 9, no. 4 (May 2004): 627–30. http://dx.doi.org/10.1177/135965350400900417.

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Standard interferon treatment is known to increase the risk of infections; this risk also needs to be evaluated in clinical practice for pegylated interferon. To this end, we studied 255 patients treated with standard (103) or pegylated (152) interferon, in combination with ribavirin, for hepatitis C. Overall, 31 anti-hepatitis C virus treatment-related infections were observed. Neutropenia (neutrophil counts below 1x103 cells/ml) was observed in a significantly higher proportion of patients treated with pegylated interferons (48% vs 9%; P=0.0009). Of the 31 infections, eight were respiratory infections and were observed only in patients with neutropenia. None of the non-respiratory infections was observed in patients with neutropenia. Multivariate analysis, using Cox's proportional hazards regression model, found a higher risk of all infections associated with both use of pegylated interferons [hazard ratio (HR) 4.6] and neutropenia (HR 2.46). However, neutropenia was independently associated with acute respiratory infections only and use of pegylated interferons with non-respiratory infections. In summary, use of pegylated interferon appears to increase the risk of non-respiratory infections independently from neutropenia.

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Hamilton, A. O., L. Jones, L. Morrison, and K. Whaley. "Modulation of monocyte complement synthesis by interferons." Biochemical Journal 242, no. 3 (March 15, 1987): 809–15. http://dx.doi.org/10.1042/bj2420809.

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Recombinant Escherichia coli-derived gamma-interferon has been shown to stimulate synthesis of the second component of complement (C2), factor B and C1 inhibitor, but to inhibit synthesis of the third component (C3). alpha- and beta-interferons stimulate synthesis of factor B and C3 inhibitor, inhibit C5 synthesis but do not alter synthesis of C2. alpha- and beta-interferons act synergistically with gamma-interferon to enhance both factor B and C1-inhibitor synthesis.

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Joyce, Margaret M., Robert C. Burghardt, Rodney D. Geisert, James R. Burghardt, R. Neil Hooper, Jason W. Ross, Morgan D. Ashworth, and Greg A. Johnson. "Pig Conceptuses Secrete Estrogen and Interferons to Differentially Regulate Uterine STAT1 in a Temporal and Cell Type-Specific Manner." Endocrinology 148, no. 9 (September 1, 2007): 4420–31. http://dx.doi.org/10.1210/en.2007-0505.

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Conceptus trophectoderm and uterine luminal epithelial cells interact via endocrine, paracrine, and autocrine modulators to mediate pregnancy recognition and implantation. Pig conceptuses not only release estrogens for pregnancy recognition but also secrete interferons during implantation. Because interferon-stimulated genes are increased by interferons secreted for pregnancy recognition in ruminants, we asked whether the interferon-stimulated gene, STAT1, is up-regulated in pig endometrium by conceptus estrogens and/or interferons. STAT1 expression in response to day of pregnancy, estrogen injection, and intrauterine infusion of conceptus secretory proteins in pigs indicated 1) estrogen increases STAT1 in luminal epithelial cells, 2) conceptus secretory proteins that contain interferons increase STAT1 in stroma, 3) STAT1 increases in close proximity to the conceptus, and 4) early estrogen results in conceptus death and no STAT1 in stroma. The interactions of estrogen and interferons to regulate cell-type-specific expression of STAT1 highlight the complex interplay between endometrium and conceptus for pregnancy recognition and implantation.

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Aschacher, Thomas, Artem Krokhin, Irina Kuznetsova, Johannes Langle, Vladimir Nebolsin, Andrey Egorov, and Michael Bergmann. "Effect of the preparation Ingavirin® (imidazolyl ethanamide pentandioic acid) on the interferon status of cells under conditions of viral infection." Epidemiology and Infectious Diseases 21, no. 4 (August 15, 2016): 196–205. http://dx.doi.org/10.17816/eid40907.

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Ingavirin® (imidazolyl ethanamide pentandioic acid) is an original antiviral drug, which is used in Russia for treatment and profilaxis of influenza and other acute viral infections. We confirmed that imidazolyl ethanamide pentandioic acid (IEPA), not being interferon inducer itself, enhances synthesis of both interferon-a/fi receptors (IFNAR) to interferone and cell sensitivity to interferone signalling, which was suppressed by NS1 protein - pathogen factor of influenza virus. IEPA is able to promote antiviral effector proteins PKR and MxA in infected cells, in opposition to interferon system suppression by influenza virus. Theoretical ground of clinical efficacy of Ingavirine® could be confirmed by obtained data of influence to innate immune system during viral infection.

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Domeier, Phillip P., and Ziaur S. M. Rahman. "Regulation of B Cell Responses in SLE by Three Classes of Interferons." International Journal of Molecular Sciences 22, no. 19 (September 28, 2021): 10464. http://dx.doi.org/10.3390/ijms221910464.

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There are three classes of interferons (type 1, 2, and 3) that can contribute to the development and maintenance of various autoimmune diseases, including systemic lupus erythematosus (SLE). Each class of interferons promotes the generation of autoreactive B cells and SLE-associated autoantibodies by distinct signaling mechanisms. SLE patients treated with various type 1 interferon-blocking biologics have diverse outcomes, suggesting that additional environmental and genetic factors may dictate how these cytokines contribute to the development of autoreactive B cells and SLE. Understanding how each class of interferons controls B cell responses in SLE is necessary for developing optimized B cell- and interferon-targeted therapeutics. In this review, we will discuss how each class of interferons differentially promotes the loss of peripheral B cell tolerance and leads to the development of autoreactive B cells, autoantibodies, and SLE.

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Galik, P. K., J. A. Gard, T. S. Spencer, M. S. Marley, D. A. Stringfellow, M. D. Givens, and M. A. Edmondson. "153 EFFECTS OF OVINE INTERFERON-β ON REPLICATION OF BOVINE VIRAL DIARRHEA VIRUS AND BOVINE HERPESVIRUS-1." Reproduction, Fertility and Development 20, no. 1 (2008): 156. http://dx.doi.org/10.1071/rdv20n1ab153.

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Bovine viral diarrhea virus (BVDV) and bovine herpesvirus-1 (BHV-1) are the most commonly isolated viruses from abattoir-origin materials utilized in embryo production and known to associate with zona pellucida-intact (ZP-I) embryos after exposure and washing. Some evidence indicates that developing embryos may produce substances that are able to inhibit viral replication in adjacent cells. Interferons such as recombinant human interferon-α are known to have anti-BVDV activity but no effect against BHV-1. In some preliminary studies, bovine interferon-τ has shown antiviral activities against BVDV but not against BHV-1. However, interferon-τ in other species has not been evaluated for anti-BVDV and anti-BHV-1 effects. Thus, the objective of this study was to evaluate the cytotoxicity and anti-viral effect of ovine interferon-τ against a non-cytopathic high affinity strain of BVDV (SD-1) and BHV-1 (Colorado) in cell culture. Serial dilutions (1:10) beginning with an initial concentration of 1 mg mL–1 of interferon-τ were made in 96-well plates and then Madin Darby bovine kidney (MDBK) cells were seeded in the wells. Cells and interferon-τ were incubated at 37.5�C in 5% CO2 and air for 24 h prior to addition of virus. The following concentrations of BVDV were added to the wells: 6000, 3500, 1000, 625, and 350 cell culture infective doses (CCID50) (50% endpoint) per well. In addition, four viral concentrations of BHV-1, 1000, 500, 250, and 100 CCID50/mL were evaluated in separate cell cultures. Virus isolation was utilized to determine if the addition of interferon-τ decreased the amount of infective virus. Ovine interferon-τ produced no observable cytotoxicity in MDBK cells in any of the assays. Also, the three highest concentrations of interferon-τ significantly decreased the amount of BVDV in all of the concentrations of BVDV tested but had no apparent effect on the concentration of BHV-1 in cell cultures. Therefore ovine interferon-τ has anti-BVDV effects similar to those seen with bovine interferont-τ and neither has any apparent antiviral activity on BHV-1 in cell culture. Additionally, ovine and bovine interferon-τ might serve to limit or prevent the transmission of BVDV and curtail the negative effects of BVDV on oocyte and embryo development. However, a similar effect is not expected for BHV-1.

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Ramaswamy, Madhu, Raj Tummala, Katie Streicher, Andre Nogueira da Costa, and Philip Z. Brohawn. "The Pathogenesis, Molecular Mechanisms, and Therapeutic Potential of the Interferon Pathway in Systemic Lupus Erythematosus and Other Autoimmune Diseases." International Journal of Molecular Sciences 22, no. 20 (October 19, 2021): 11286. http://dx.doi.org/10.3390/ijms222011286.

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Therapeutic success in treating patients with systemic lupus erythematosus (SLE) is limited by the multivariate disease etiology, multi-organ presentation, systemic involvement, and complex immunopathogenesis. Agents targeting B-cell differentiation and survival are not efficacious for all patients, indicating a need to target other inflammatory mediators. One such target is the type I interferon pathway. Type I interferons upregulate interferon gene signatures and mediate critical antiviral responses. Dysregulated type I interferon signaling is detectable in many patients with SLE and other autoimmune diseases, and the extent of this dysregulation is associated with disease severity, making type I interferons therapeutically tangible targets. The recent approval of the type I interferon-blocking antibody, anifrolumab, by the US Food and Drug Administration for the treatment of patients with SLE demonstrates the value of targeting this pathway. Nevertheless, the interferon pathway has pleiotropic biology, with multiple cellular targets and signaling components that are incompletely understood. Deconvoluting the complexity of the type I interferon pathway and its intersection with lupus disease pathology will be valuable for further development of targeted SLE therapeutics. This review summarizes the immune mediators of the interferon pathway, its association with disease pathogenesis, and therapeutic modalities targeting the dysregulated interferon pathway.

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Lucivero, G. "The Interferons in Clinical Practice." International Journal of Immunopathology and Pharmacology 5, no. 2 (May 1992): 83–92. http://dx.doi.org/10.1177/039463209200500203.

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In the last decade, recombinant DNA technologies have allowed the production of highly purified interferons in virtually unlimited amounts. Therefore it has become possible to evaluate the usefulness of interferon therapy in several different diseases. Nowadays interferons have a well defined role in the therapy of infectious and malignant diseases. As these natural modifiers of biological responses are widely available to the specialist and to the general practitioner as well, in the present paper we review the main biochemical properties and the molecular mechanisms underlying the heterogeneous activities of the interferons. Furthermore, on the basis of already published therapeutical trials, we indicate the infectious and neoplastic diseases in which therapy with interferon has been effective and outline the most frequent toxic or side effects of this therapy.

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Rogovaya, O. C., L. Sh Izmaylova, and O. O. Serbina. "Assessment of the antiproliferative effect of antiviral drugs." Infekcionnye bolezni 18, no. 2 (2020): 48–56. http://dx.doi.org/10.20953/1729-9225-2020-2-48-56.

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Yum, Seoyun, Minghao Li, Yan Fang, and Zhijian J. Chen. "TBK1 recruitment to STING activates both IRF3 and NF-κB that mediate immune defense against tumors and viral infections." Proceedings of the National Academy of Sciences 118, no. 14 (March 30, 2021): e2100225118. http://dx.doi.org/10.1073/pnas.2100225118.

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The induction of type I interferons through the transcription factor interferon regulatory factor 3 (IRF3) is considered a major outcome of stimulator of interferon genes (STING) activation that drives immune responses against DNA viruses and tumors. However, STING activation can also trigger other downstream pathways such as nuclear factor κB (NF-κB) signaling and autophagy, and the roles of interferon (IFN)-independent functions of STING in infectious diseases or cancer are not well understood. Here, we generated a STING mouse strain with a mutation (S365A) that disrupts IRF3 binding and therefore type I interferon induction but not NF-κB activation or autophagy induction. We also generated STING mice with mutations that disrupt the recruitment of TANK-binding kinase 1 (TBK1), which is important for both IRF3 and NF-κB activation but not autophagy induction (L373A or ∆CTT, which lacks the C-terminal tail). The STING-S365A mutant mice, but not L373A or ∆CTT mice, were still resistant to herpes simplex virus 1 (HSV-1) infections and mounted an antitumor response after cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) treatment despite the absence of STING-induced interferons. These results demonstrate that STING can function independently of type I interferons and autophagy, and that TBK1 recruitment to STING is essential for antiviral and antitumor immunity.

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Tiwari, R. K., J. Kusari, R. Kumar, and G. C. Sen. "Gene induction by interferons and double-stranded RNA: selective inhibition by 2-aminopurine." Molecular and Cellular Biology 8, no. 10 (October 1988): 4289–94. http://dx.doi.org/10.1128/mcb.8.10.4289-4294.1988.

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Transcription of several interferon-inducible human genes is also induced by double-stranded RNA. The nature and the mechanism of action of signals generated by interferons and by double-stranded RNA which mediate the induction of these genes are under investigation. Here we report that 2-aminopurine, a known inhibitor of protein kinases, could selectively block this induction process. Induction of mRNAs 561 and 6-16 in HeLaM cells by double-stranded RNA was completely inhibited by 10 mM 2-aminopurine, whereas cellular protein and RNA syntheses as well as the induction of metallothionein mRNA by CdCl2 were unaffected by this inhibitor. In addition, 2-aminopurine blocked the induction of the same two mRNAs and of mRNAs 2-5(A) synthetase, 2A, and 1-8 by alpha interferon and of mRNAs 2A and 1-8 by gamma interferon in HeLaM cells. The observed inhibition was at the level of transcription, and for establishing efficient inhibition, the 2-aminopurine treatment had to begin at early stages of interferon treatment. In GM2767 cells, 2-aminopurine inhibited induction of mRNAs 561 and 6-16 by double-stranded RNA but not by alpha interferon. These results suggest that double-stranded RNA-induced signal 2 is distinct from the interferon-alpha-induced signal 2 (R. K. Tiwari, J. Kusari, and G. C. Sen, EMBO J. 6:3373-3378, 1987) and that 2-aminopurine can block the former but not the latter. Moreover, it appeared that 2-aminopurine could block the production of signal 1 by interferons. This was confirmed by experiments in which we separately tested the effects of 2-aminopurine on signal 1 and signal 2 production by interferons in HeLaM cells. Although no direct experimental evidence is available as yet, our results are consistent with the hypothesis that the functioning of a protein kinase activity may be necessary for transcriptional induction of genes by double-stranded RNA and for gene induction by interferons in those cells in which signal 1 production is needed.

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Tiwari, R. K., J. Kusari, R. Kumar, and G. C. Sen. "Gene induction by interferons and double-stranded RNA: selective inhibition by 2-aminopurine." Molecular and Cellular Biology 8, no. 10 (October 1988): 4289–94. http://dx.doi.org/10.1128/mcb.8.10.4289.

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Transcription of several interferon-inducible human genes is also induced by double-stranded RNA. The nature and the mechanism of action of signals generated by interferons and by double-stranded RNA which mediate the induction of these genes are under investigation. Here we report that 2-aminopurine, a known inhibitor of protein kinases, could selectively block this induction process. Induction of mRNAs 561 and 6-16 in HeLaM cells by double-stranded RNA was completely inhibited by 10 mM 2-aminopurine, whereas cellular protein and RNA syntheses as well as the induction of metallothionein mRNA by CdCl2 were unaffected by this inhibitor. In addition, 2-aminopurine blocked the induction of the same two mRNAs and of mRNAs 2-5(A) synthetase, 2A, and 1-8 by alpha interferon and of mRNAs 2A and 1-8 by gamma interferon in HeLaM cells. The observed inhibition was at the level of transcription, and for establishing efficient inhibition, the 2-aminopurine treatment had to begin at early stages of interferon treatment. In GM2767 cells, 2-aminopurine inhibited induction of mRNAs 561 and 6-16 by double-stranded RNA but not by alpha interferon. These results suggest that double-stranded RNA-induced signal 2 is distinct from the interferon-alpha-induced signal 2 (R. K. Tiwari, J. Kusari, and G. C. Sen, EMBO J. 6:3373-3378, 1987) and that 2-aminopurine can block the former but not the latter. Moreover, it appeared that 2-aminopurine could block the production of signal 1 by interferons. This was confirmed by experiments in which we separately tested the effects of 2-aminopurine on signal 1 and signal 2 production by interferons in HeLaM cells. Although no direct experimental evidence is available as yet, our results are consistent with the hypothesis that the functioning of a protein kinase activity may be necessary for transcriptional induction of genes by double-stranded RNA and for gene induction by interferons in those cells in which signal 1 production is needed.

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Pestka, Sidney, Christopher D. Krause, and Mark R. Walter. "Interferons, interferon-like cytokines, and their receptors." Immunological Reviews 202, no. 1 (December 2004): 8–32. http://dx.doi.org/10.1111/j.0105-2896.2004.00204.x.

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Gun, Sin Yee, Carla Claser, Kevin Shyong Wei Tan, and Laurent Rénia. "Interferons and Interferon Regulatory Factors in Malaria." Mediators of Inflammation 2014 (2014): 1–21. http://dx.doi.org/10.1155/2014/243713.

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Malaria is one of the most serious infectious diseases in humans and responsible for approximately 500 million clinical cases and 500 thousand deaths annually. Acquired adaptive immune responses control parasite replication and infection-induced pathologies. Most infections are clinically silent which reflects on the ability of adaptive immune mechanisms to prevent the disease. However, a minority of these can become severe and life-threatening, manifesting a range of overlapping syndromes of complex origins which could be induced by uncontrolled immune responses. Major players of the innate and adaptive responses are interferons. Here, we review their roles and the signaling pathways involved in their production and protection against infection and induced immunopathologies.

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Samuel, Charles E., and Keiko Ozato. "Induction of interferons and interferon-induced genes." Biotherapy 8, no. 3-4 (September 1996): 183–87. http://dx.doi.org/10.1007/bf01877203.

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Brzoska, Josef, Harald von Eick, and Manfred Hündgen. "Interferons in the Therapy of Severe Coronavirus Infections: A Critical Analysis and Recollection of a Forgotten Therapeutic Regimen with Interferon Beta." Drug Research 70, no. 07 (May 22, 2020): 291–97. http://dx.doi.org/10.1055/a-1170-4395.

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AbstractThe pharmacological and immunological properties of interferons, especially those of interferon beta, and the corresponding treatment strategies are described, and the results of studies with different interferons in coronavirus infections are analysed. Furthermore, the data obtained with high-dosed native interferon beta in life-threatening acute viral diseases as well as the results of clinical pilot studies with high-dosed recombinant interferon beta-1a are provided because they serve as the rationale for the proposed therapeutic regimen to be applied in acute viral infections. This regimen differs from those approved for treatment of multiple sclerosis and consists of interferon beta-1a administered as a 24 hour intravenous infusion at a daily dose of up to 90 µg for 3–5 consecutive days. Since under this regimen transient severe side effects can occur, it is analysed which patients are suitable for this kind of treatment in general and if patients with severe coronavirus infections could also be treated accordingly.

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Lokshina, E. E., V. V. Malinovskaya, O. V. Zaytseva, and S. U. Snitko. "Virus-induced asthma: how to achieve good disease control?" Voprosy praktičeskoj pediatrii 15, no. 6 (2020): 52–66. http://dx.doi.org/10.20953/1817-7646-2020-6-52-66.

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This article discusses the role of various respiratory viruses in the development of bronchial asthma and in triggering its exacerbation. It covers the pathogenetic mechanisms underlying virus-induced bronchial asthma and the importance of interferons for disease control. We summarized the results of international and Russian studies analyzing the utility of type 1 interferons for children and adults with virus-induced asthma exacerbations. Combination drugs containing recombinant α2b interferon plus α-tocopheryl acetate plus ascorbic acid have demonstrated their efficacy in the prevention and treatment of virus-induced asthma exacerbations in routine clinical practice. Moreover, these drugs were safe and well tolerated by patients, which opens new prospects for patients with virus-induced asthma. Key words: virus-induced bronchial asthma, respiratory viruses, children, interferons, therapy, recombinant α2b-interferon + α-tocopheryl acetate + ascorbic acid

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Fehér, János, and Gabriella Lengyel. "Interferon in the treatment of viral hepatitis. The interferon was discovered 50 years ago." Orvosi Hetilap 148, no. 33 (August 1, 2007): 1539–43. http://dx.doi.org/10.1556/oh.2007.28194.

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Az interferonok heterogén összetételű glycoproteinek, melyeket a vírusfertőzés hatására, az immunválasz során, az élő sejtek termelnek. Felfedezésük éppen fél évszázaddal ezelőtt történt. Daganatellenes, antivirális és immunmoduláns hatásúak. A terápiában használatos interferonok görög betűkkel jelölt formái utalnak az eredetre: az interferon-alfa leukocita-eredetű, az interferon-béta fibroblastokból származó, az interferon-gamma pedig lymphocyta-eredetű immuninterferon. A humán gyógyászatban a természetes és rekombináns interferonokat egyaránt alkalmazzák. A polietilén-glikollal történő összekapcsolás az interferonkészítmény tartós hatását biztosítja. Jelenleg a klinikumban leginkább hepatitis B és C vírus okozta krónikus hepatitisben a vírus eliminálására, valamint az onkológiában daganatprogresszió gátlására alkalmazzák.

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Ahmad, Imran, Araceli Valverde, Hasan Siddiqui, Samantha Schaller, and Afsar R. Naqvi. "Viral MicroRNAs: Interfering the Interferon Signaling." Current Pharmaceutical Design 26, no. 4 (March 18, 2020): 446–54. http://dx.doi.org/10.2174/1381612826666200109181238.

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Interferons are secreted cytokines with potent antiviral, antitumor and immunomodulatory functions. As the first line of defense against viruses, this pathway restricts virus infection and spread. On the contrary, viruses have evolved ingenious strategies to evade host immune responses including the interferon pathway. Multiple families of viruses, in particular, DNA viruses, encode microRNA (miR) that are small, non-protein coding, regulatory RNAs. Virus-derived miRNAs (v-miR) function by targeting host and virus-encoded transcripts and are critical in shaping host-pathogen interaction. The role of v-miRs in viral pathogenesis is emerging as demonstrated by their function in subverting host defense mechanisms and regulating fundamental biological processes such as cell survival, proliferation, modulation of viral life-cycle phase. In this review, we will discuss the role of v-miRs in the suppression of host genes involved in the viral nucleic acid detection, JAK-STAT pathway, and cytokine-mediated antiviral gene activation to favor viral replication and persistence. This information has yielded new insights into our understanding of how v-miRs promote viral evasion of host immunity and likely provide novel antiviral therapeutic targets.

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Clynes, Raphael. "IVIG Therapy: Interfering with Interferon-γ." Immunity 26, no. 1 (January 2007): 4–6. http://dx.doi.org/10.1016/j.immuni.2007.01.006.

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Zlotorynski, Eytan. "Interfering with interferon by RNA editing." Nature Reviews Molecular Cell Biology 19, no. 3 (February 7, 2018): 141. http://dx.doi.org/10.1038/nrm.2018.12.

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Samuel, Charles E. "Interferons, Interferon Receptors, Signal Transducer and Transcriptional Activators, and Interferon Regulatory Factors." Journal of Biological Chemistry 282, no. 28 (May 14, 2007): 20045–46. http://dx.doi.org/10.1074/jbc.r700025200.

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Mazin, P. V., R. Kh Khafisyanova, N. K. Mazina, A. L. Kovalenko, and A. R. Askhadullin. "Meglumin acridonacetate to treat COVID-19: prospect of using." Infekcionnye bolezni 18, no. 4 (2020): 42–52. http://dx.doi.org/10.20953/1729-9225-2020-4-42-52.

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The use of interferon drugs against COVID-19 is based on С level of evidence and analogies with efficacy against other coronaviruses. The interferon inductor meglumin acridonacetate (Cycloferon) has an advantageous safety profile and pharmaco-economic advantages, which makes it possible to consider its probable use against SARS-CoV-2. In this review, both the evidence of the effectiveness of interferons against coronaviruses and the arguments in favor of the effectiveness of Cycloferon against the same pathogens are systematized. The arguments of pharmacodynamic, biochemical, pathophysiological experimental and clinical plan in favor of Cycloferon are presented. Key words: acridone acetic acid, Interferons, coronaviruses, COVID-19, MERS-CoV, SARS-CoV, SARS-CoV-2

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Pisanelli, Giuseppe, Ugo Pagnini, Giuseppe Iovane, and Adolfo García-Sastre. "Type I and Type II Interferon Antagonism Strategies Used by Paramyxoviridae: Previous and New Discoveries, in Comparison." Viruses 14, no. 5 (May 21, 2022): 1107. http://dx.doi.org/10.3390/v14051107.

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Paramyxoviridae is a viral family within the order of Mononegavirales; they are negative single-strand RNA viruses that can cause significant diseases in both humans and animals. In order to replicate, paramyxoviruses–as any other viruses–have to bypass an important protective mechanism developed by the host’s cells: the defensive line driven by interferon. Once the viruses are recognized, the cells start the production of type I and type III interferons, which leads to the activation of hundreds of genes, many of which encode proteins with the specific function to reduce viral replication. Type II interferon is produced by active immune cells through a different signaling pathway, and activates a diverse range of genes with the same objective to block viral replication. As a result of this selective pressure, viruses have evolved different strategies to avoid the defensive function of interferons. The strategies employed by the different viral species to fight the interferon system include a number of sophisticated mechanisms. Here we analyzed the current status of the various strategies used by paramyxoviruses to subvert type I, II, and III interferon responses.

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Popescu, L. M., C. Cernescu, I. I. Moraru, St N. Constantinescu, F. Baltã, M. Manciulea, E. Brãiloiu, and L. Buzilã. "Cell-membrane phospholipase C is involved in inducing the antiviral effect of interferon." Bioscience Reports 9, no. 5 (October 1, 1989): 531–39. http://dx.doi.org/10.1007/bf01119795.

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A monospecific inhibitory antibody directed to phospholipase C (phosphoinositidase C) blocked the antiviral effect of human interferons alpha and beta when tested on human quiescent fibroblasts challenged with the vesicular stomatitis virus. This action was due to specific inhibition of polyphosphoinositide hydrolysis because (a) the F(ab′)2 fragment of the antibody molecule was also inhibitory; (b) excess antibodies directed to phospholipase A2 and to a phosphatidylcholine-preferring phospholipase C did not have any inhibitory effect, and (c) the combination of 12-O-tetradecanoylphorbol-acetate and calcium ionophore A23187 had an interferon-like antiviral effect which was not influenced by the inhibitory anti-phospholipase C antibodies. To avoid an interferon-like effect due to induction of interferon by second messengers, Vero cells, which lack interferon biosynthesis, were also used. Liposomes containing inositol 1,4,5-triphosphate and 1-oleoyl-2-acetyl-rac-glycerol protected Vero cells against the infection with the vesicular stomatitis virus. These results taken together show that phosphoinositide-derived second messengers are involved in triggering the antiviral effect of interferons alpha and beta.

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Obar, Joshua J., Alayna Katherine Caffrey, Xi Wang, Vanessa Espinosa, Yi-Wei Tang, Tobias Hohl, Amariliz Rivera, and Robert Cramer. "Mda5/MAVS signaling is essential for resistance against Aspergillus fumigatus." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 52.23. http://dx.doi.org/10.4049/jimmunol.200.supp.52.23.

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Abstract Type I and III interferons act as important activators of antifungal neutrophil response in the lungs. The RIG-I like receptor (RLR) family, including RIG-I and Mda5, are cytosolic RNA sensors that signal through the MAVS adaptor in order to activate interferon responses against viruses. Whether the RLR family has broader effects on host immunity against other pathogen families remains to be fully explored. Herein we demonstrate that Mda5/MAVS signaling was essential for host resistance against pulmonary Aspergillus fumigatus challenge through the regulation of antifungal leukocyte responses. Aspergillus fumigatus induction of type I interferons was partially dependent on Mda5/MAVS signaling, while type III interferon expression was entirely dependent on Mda5/MAVS signaling. Activation of the interferon pathway was driven by prolonged exposure to fungal spores, rather than germ tubes. Ultimately, interferon signaling drove the expression of CXCL9 and CXCL10, SNPs in the latter are associated with invasive aspergillosis in human patients. Our data suggest a broader role of the RLR family in the regulation of innate immunity to include invasive fungal infections.

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Journal articles on the topic 'Interferoni'

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