Ask about this productRelated genes to: IRF8 Blocking Peptide
- Gene:
- IRF8 NIH gene
- Name:
- interferon regulatory factor 8
- Previous symbol:
- ICSBP1
- Synonyms:
- IRF-8, ICSBP
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-09
- Date modifiied:
- 2019-04-23
Related products to: IRF8 Blocking Peptide
Related articles to: IRF8 Blocking Peptide
- Primary cutaneous follicle center lymphomas (PCFCLs) are indolent B-cell neoplasms limited to the skin and effectively managed with local therapies. Distinguishing PCFCL from systemic follicular lymphoma (sFL) with cutaneous involvement (FL_CI) is challenging due to overlapping features. We performed an integrated pathological and genetic analysis of skin samples of 24 PCFCL and 10 FL_CI, which showed subtle pathological changes (decreased BCL2 and CD10, increased CD23 expression in PCFCL), but markedly distinct mutational landscapes. FL_CI exhibited recurrent mutations in chromatin-modifying genes ( 90%, 90%, and 30%), closely resembling sFL. In contrast, PCFCL displayed a more heterogeneous profile, with mutations affecting B-cell development, cell adhesion, and immune evasion. These molecular alterations identified three distinct PCFCL subgroups. Group 1 (44%) harbored mutations in immune evasion genes (, , , and ) and was associated with CD10 negativity, diffuse architecture, and localization in non-photoexposed areas. Group 2 (20%) showed activating and mutations, consistent CD23 and CD10 positivity, and exclusive presentation in sun-exposed sites. Group 3 (20%) shared a similar clinicopathological profile to Group 2 but was defined by mutations. Clonal origin and mutational evolution were studied in five patients, one with synchronous PCFCL and four with sequential samples from two PCFCL and 2 FL_CI. This analysis supports a model of PCFCL oncogenesis driven by circulating progenitors following complex evolutionary patterns, including convergent evolution and greater clonal diversity at relapse. Overall, our study refines the mechanisms driving PCFCL pathogenesis, while providing a framework for PCFCL differential diagnosis and clinical management. - Source: PubMed
Publication date: 2026/05/29
Combalia AndreaVidal-Robau NuriaNadeu FerranLópez CristinaFrigola GerardLopez-Oreja IreneGarcia NoeliaBashiri MelikaMozas PabloLopez-Guillermo ArmandoSalaverria ItziarEstrach TeresaCampo EliasGarcia-Herrera AdrianaAlbero Robert - Interleukin (IL)-33 is a pleiotropic cytokine in the immune system and inflammatory responses, which is involved in cerebral ischemia/reperfusion (I/R) injury. Evidence indicates that IL-33 plays an essential role in macrophage polarization activation, yet the potential molecular mechanisms remain elusive. This study explored the role of IL-33 in the activation of microglia/macrophage-mediated autophagy for cerebral I/R injury via in vitro experiments. - Source: PubMed
Publication date: 2026/01/23
Yong FanLili LinKailiang HuangJinying LinJunping XuXiaohui ZhouYongkai Yang - : Type 1 diabetes (T1D) and multiple sclerosis (MS) are autoimmune, multifactorial, organ-specific disorders mediated by immune cells. Their co-occurrence has been partially attributed to shared genetics and environmental factors. We aimed to dissect the shared genetic architecture between T1D and MS using large-scale genome-wide association studies (GWASs) and colocalization analyses. : We applied a Bayesian colocalization framework to two large-scale GWAS data sets: a T1D study comprising 18,942 cases and 501,638 controls, and an MS GWAS including 14,802 cases and 26,703 controls. : We identified 26 shared colocalizing association signals between T1D and MS. Among them, seven loci (, , , , , , and ) were novel for T1D and two ( and ) for MS. Several signals showed supportive evidence in additional datasets and demonstrated functional annotation characteristics consistent with disease involvement. : Colocalization can be a powerful discovery tool for disorders with co-divided genetic architecture, as prioritizing shared rather than individual causal variants may enhance the detection of novel loci. Our findings indicate that T1D and MS predominantly share general autoimmune susceptibility signals (17/26), rather than disease-specific (private), often with opposite direction of effect (9/26), underscoring their immunological heterogeneity. - Source: PubMed
Publication date: 2026/04/30
Steri MaristellaTestori AlessandroOrrù ValeriaZoledziewska Magdalena - The genetic architecture of B-cell lymphomas is not fully characterized. We aimed to identify novel candidate variants associated with four common B-cell lymphoma subtypes-diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), chronic lymphocytic leukemia (CLL), and marginal zone lymphoma (MZL)-through cross-trait analyses with correlated idiopathic inflammatory myopathies subtypes, dermatomyositis (DM) and polymyositis (PM). Leveraging shared genetic susceptibility with DM and PM, we applied a pleiotropy-informed conditional false discovery rate (condFDR) method to recompute nominal single nucleotide polymorphism association -values for each B-cell lymphoma subtype. Associations were considered significant at condFDR <0.01. Functional annotation was performed using FUMA (Functional Mapping and Annotation of Genome-Wide Association Studies), followed by Gene Ontology (GO) enrichment analysis via clusterProfiler, with similar GO terms clustered for interpretation and visualization. We identified 4, 2, 13, and 6 novel candidate loci for DLBCL, FL, CLL, and MZL, respectively. Most loci exhibited regulatory effects on genes involved in adaptive immune responses and cell death pathways. Notably, for DLBCL locus 1q23.3 affects SLAMF genes implicated in natural killer and lymphocyte activation. A trans-eQTL at 2q13 for FL was associated with BCL11A, a multifunctional oncogene. For CLL, a novel locus at 16q24.1 regulates IRF8, a known CLL risk gene. Functional mapping of previously reported CLL risk loci revealed RIPK1 (6p25.2), linked to necroptosis. No enriched biological pathways were detected for MZL risk-associated genes. These findings advance our understanding of the genetic architecture of four B-cell lymphoma subtypes and aim to inform future genetic and functional studies. - Source: PubMed
Publication date: 2026/05/09
Che Weng IanJarvis James NInternational Lymphoma Epidemiology Consortium InterLymph Imacs Genetics Group Myogen Lundberg Ingrid ESmedby Karin ELamb Janine AHolmqvist Marie - Microglia rapidly respond to injury, stress, and perturbations to neurons in the brain and retina and perform phagocytosis to clear dying cells and debris. Oxidative stress is a feature of neurodegeneration, and while glia are crucial for managing such stress, microglia may also be dysfunctional in diseased tissue. Here we examine the role of microglia in management of oxidative stress and restoring redox homeostasis following death of rod photoreceptors in the larval zebrafish retina. Using rho:nfsb-eGFP transgenic zebrafish and treatment with the pro-drug metronidazole (MTZ), we coupled the generation of reactive oxygen species (ROS) in dying rods to their ablation. Microglia efficiently engulfed and cleared the ROS-laden rods, effectively undertaking the oxidative load. Despite abundant ROS upon MTZ-mediated cell death, oxidative stress overall was minimal in retinal tissue when microglia were present, indicating that they rapidly and efficiently performed redox functions. In irf8-/- mutants, which are deficient in microglia, retinas with MTZ-induced rod ablation showed widespread ROS that localized, at least in part, to Müller glia. Microglia deficient retinas showed evidence of increased oxidative stress, and increased numbers of "off-target" inner retinal neurons that stained positive for the cell death marker TUNEL. Supplementation with the antioxidant Glutathione modestly reduced the number of off-target TUNEL+ cells detected in microglia-deficient retinas following rod ablation. We also found that microglia may be important for mitigating effects of MTZ alone in the absence of Nfsb enzyme. Our results suggest that microglial redox functions are important in maintaining and restoring homeostasis following acute retinal damage. - Source: PubMed
Publication date: 2026/05/18
Morales MichaelMitchell Diana M