The interferons alpha, beta, and w (IFNA, IFNB, IFNW), are a family of genes that have been mapped on the short arm of chromosome 9 (9p21-22). Deletions of genetic material on 9p are frequently observed in hematological diseases, particularly in lymphoid neoplasias. In this paper we have performed the molecular studies of IFNA and IFNB genes in chronic myeloid leukemia (CML) in order to determine if the deletions of these genes are prevalent in this pathology. Forty CML patients, Philadelphia positive or with BCR/ABL rearrangement, were studied at diagnosis. The analysis of IFNA and IFNB genes was performed by Southern and dot blot techniques. Homozygous or hemizygous deletions of IFNA and IFNB genes could not be detected, indicating that deletions of these genes would not be present or would be a very infrequent event in the chronic phase of the CML patients.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0145-2126(95)00010-l | DOI Listing |
Front Immunol
January 2025
Norwegian College of Fishery Science, Faculty of Bioscience, Fisheries and Economics, University of Tromsø - The Arctic University of Norway, Tromsø, Norway.
Non-classical MHC class I genes which, compared to classical MHC class I, are typically less polymorphic and have more restricted expression patterns are attracting interest because of their potential to regulate immune responses to various pathogens. In salmonids, among the numerous non-classical MHC class I genes identified to date, L lineage genes, including Sasa- and , are differentially induced in response to microbial challenges. In the present study, we show that while transcription of both and are induced in response to SAV3 infection the transcriptional induction patterns are distinct for each gene.
View Article and Find Full Text PDFVet Immunol Immunopathol
December 2024
National Reference Center of Veterinary and Comparative Oncology (CEROVEC), Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Genova 16129, Italy. Electronic address:
Swine are considered one of the most relevant large animal biomedical models since they share many immunological similarities with humans. Despite that, macrophage polarization has not comprehensively investigated in pigs. In this study, porcine monocyte-derived macrophages (moMΦ) were untreated or stimulated with IFN-γ + LPS (classical activation), or by different M2 polarizing stimuli: IL-4, IL-10, TGF-β, or dexamethasone.
View Article and Find Full Text PDFCell Mol Life Sci
August 2024
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, Seoul, 03080, Korea.
While severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is characterized by impaired induction of interferons (IFNs) and IFN-stimulated genes (ISGs), the IFNs and ISGs in upper airway is essential to restrict the spread of respiratory virus. Here, we identified the prominent IFN and ISG upregulation in the nasopharynx (NP) of mild and even severe coronavirus disease 2019 (COVID-19) patients (CoV2+) in Omicron era and to compare their clinical outcome depending on the level of IFNs and ISGs. Whereas the induction of IFNB was minimal, transcription of IFNA, IFNG, and IFNLs was significantly increased in the NP of CoV2 + patients.
View Article and Find Full Text PDFFish Shellfish Immunol
August 2024
Norwegian College of Fishery Science, UiT the Arctic University of Norway, 9037, Tromsø, Norway.
Type I interferons (IFN-I) play a pivotal role in vertebrate innate immunity against viruses. This study is an analysis of IFN-I genes in an updated version of the Atlantic salmon genome published in 2021 (version Ssal_v3.1), revealing 47 IFN-I genes in the Atlantic salmon genome.
View Article and Find Full Text PDFSci Signal
April 2024
Department of Surgery, College of Medicine, Cancer Center, University of Illinois at Chicago, Chicago, IL 60612, USA.
Type I interferons (IFNs) are critical for the antiviral immune response, and fine-tuning type I IFN production is critical to effectively clearing viruses without causing harmful immunopathology. We showed that the transcription factor Miz1 epigenetically repressed the expression of genes encoding type I IFNs in mouse lung epithelial cells by recruiting histone deacetylase 1 (HDAC1) to the promoters of and . Loss of function of Miz1 resulted in augmented production of these type I IFNs during influenza A virus (IAV) infection, leading to improved viral clearance in vitro and in vivo.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!