ReviewBiology2021
IFP35 Is a Relevant Factor in Innate Immunity, Multiple Sclerosis, and Other Chronic Inflammatory Diseases: A Review.
Review in Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- N-myc and STAT interactor is a novel biomarker for predicting the severity and clinical outcome of sepsis: a prospective research.Frontiers in cellular and infection microbiology · 2026Article
- The Age-Related Efficacy of Dimethyl Fumarate in Naive Versus Switcher Multiple Sclerosis Patients: A Multicenter Population-Based Study.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Article
- Kynurenine Pathway Modulation by Exercise in Multiple Sclerosis: Implications for Neuroprotection and Inflammation.Cellular and molecular neurobiology · 2025Review
- NET Proteomic Profiling Reveals New Pathways Potentially Implicated in Dendritic Cell-Mediated Inflammation in DADA2 Patients.Journal of clinical immunology · 2025Article
- The role of BATF in immune cell differentiation and autoimmune diseases.Biomarker research · 2025Review
- IRF3 regulates neuroinflammatory responses and the expression of genes associated with Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Ultrastructural Characterization of PBMCs and Extracellular Vesicles in Multiple Sclerosis: A Pilot Study.International journal of molecular sciences · 2024Article
- The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model.Viruses · 2023Review
- Multi-Criterial Model for Weighting Biological Risk Factors in Multiple Sclerosis: Clinical and Health Insurance Implications.Healthcare (Basel, Switzerland) · 2023Article
- Knockdown of KLF5 ameliorates renal fibrosis in MRL/lpr mice via inhibition of MX1 transcription.Immunity, inflammation and disease · 2023Article
- Characterisation of key biomarkers in diabetic ulcers via systems bioinformatics.International wound journal · 2023Article
- Identification and characterization of RBM12 as a novel regulator of fetal hemoglobin expression.Blood advances · 2022Article
- Identifying key genes in CD4Frontiers in genetics · 2022Article
- Expression and mechanisms of interferon-stimulated genes in viral infection of the central nervous system (CNS) and neurological diseases.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Discovered in 1993 by Bange et al., the 35-kDa interferon-induced protein (IFP35) is a highly conserved cytosolic interferon-induced leucine zipper protein with a 17q12-21 coding gene and unknown function. Belonging to interferon stimulated genes (ISG), the IFP35 reflects the type I interferon (IFN) activity induced through the JAK-STAT phosphorylation, and it can homodimerize with N-myc-interactor (NMI) and basic leucine zipper transcription factor (BATF), resulting in nuclear translocation and a functional expression. Casein kinase 2-interacting protein-1 (CKIP-1), retinoic acid-inducible gene I (RIG-I), and laboratory of genetics and physiology 2 Epinephelus coioides (EcLGP2) are thought to regulate IFP35, via the innate immunity pathway. Several in vitro and in vivo studies on fish and mammals have confirmed the IFP35 as an ISG factor with antiviral and antiproliferative functions. However, in a mice model of sepsis, IFP35 was found working as a damage associated molecular pattern (DAMP) molecule, which enhances inflammation by acting in the innate immune-mediated way. In human pathology, the IFP35 expression level predicts disease outcome and response to therapy in Multiple Sclerosis (MS), reflecting IFN activity. Specifically, IFP35 was upregulated in Lupus Nephritis (LN), Rheumatoid Arthritis (RA), and untreated MS. However, it normalized in the MS patients undergoing therapy. The considered data indicate IFP35 as a pleiotropic factor, suggesting it as biologically relevant in the innate immunity, general pathology, and human demyelinating diseases of the central nervous system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.