Human Interleukin 28B,IL-28B ELISA Kit
- Known as:
- Human Interleukin 28B,Interleukin-28B Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-0042
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Interleukin 28B IL-28B ELISA Kit
Related genes to: Human Interleukin 28B,IL-28B ELISA Kit
- Gene:
- IFNL3 NIH gene
- Name:
- interferon lambda 3
- Previous symbol:
- IL28B
- Synonyms:
- IL-28B, IL28C
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-02
- Date modifiied:
- 2019-04-23
- Gene:
- IFNL3P1 NIH gene
- Name:
- interferon lambda 3 pseudogene 1
- Previous symbol:
- IL28BP1
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- pseudogene
- Date approved:
- 2012-11-07
- Date modifiied:
- 2016-06-13
Related products to: Human Interleukin 28B,IL-28B ELISA Kit
Related articles to: Human Interleukin 28B,IL-28B ELISA Kit
- Type III interferons (IFNλs) represent the newest interferon family, comprising four human subtypes (IFNλ1-4) that signal through the tissue-restricted IFNLR1 receptor. While traditionally characterized as antiviral cytokines protecting mucosal barriers, accumulating evidence suggests that IFNλs possess broader physiological roles that remain incompletely understood. A critical gap in our knowledge concerns whether the four IFNλ subtypes function redundantly, or serve distinct biological purposes. Recent discoveries challenge the assumption of functional redundancy among IFNλ subtypes. Emerging data indicate that different subtypes exhibit distinct signaling kinetics, potencies, and downstream effects on epithelial biology. Beyond their established antiviral functions, IFNλs appear to regulate fundamental aspects of epithelial homeostasis, including barrier integrity, cellular differentiation, and tissue architecture. The discovery of constitutive basal IFNλ expression in healthy epithelia-driven by microbiota and endogenous danger signals-suggests that these cytokines continuously shape tissue physiology rather than functioning solely as inducible defense molecules. Understanding subtype-specific IFNλ functions has become increasingly urgent as these cytokines enter clinical development. The tissue-restricted expression of IFNLR1 offers therapeutic advantages over broadly-acting type I interferons, but optimal clinical application requires comprehensive knowledge of how individual subtypes influence both pathogen control and tissue homeostasis. Critical questions remain: Do specific subtypes preferentially regulate barrier function versus antiviral immunity? Can imbalanced subtype expression contribute to epithelial pathology? How do pathogens differentially induce IFNλ subtypes to evade immunity or promote tissue damage? Addressing these questions will illuminate fundamental principles of mucosal immunity and guide rational design of IFNλ-based therapeutics that maximize protection while preserving epithelial health. - Source: PubMed
Publication date: 2026/06/02
Stanifer Megan L - Lambda interferons signal through the interferon lambda receptor 1 (IFNLR1) and IL10RB heterodimer to induce interferon stimulated genes (ISGs). We previously showed that proteins derived from distinct IFNLR1 splice isoforms uniquely influence gene expression and hepatitis B virus replication in stem cell-derived hepatocytes (iHeps). Here, we evaluated signal transduction mechanisms of full-length IFNLR1 (variant 1) and a truncated variant missing part of the cytoplasmic JAK1-interacting domain (variant 2). - Source: PubMed
Publication date: 2026/05/29
Novotny Laura AMartinez-Morant CarlaDuncan Stephen ATraktman PaulaGooz MonikaMeissner Eric G - The type III interferon family, known as interferon lambda (IFN-λ), consists of four isoforms (IFN-λ1, IFN-λ2, IFN-λ3, and IFN-λ4) and plays essential roles in immune responses. It mediates anti-viral and anti-tumoral activities and is distinguished from type I and type II interferons (IFNs) by its interaction with a unique receptor complex involving IFN-λR1 and IL-10 Rβ predominantly expressed on epithelial cells and selected immune cell populations. This interaction results in activation of the JAK-STAT signaling pathway and transcription of interferon-stimulated genes (ISGs). - Source: PubMed
Publication date: 2026/05/06
Blümke JulianeSeliger Barbara - Invariant natural killer T (iNKT) cells play a critical role in the early phases of the response to Influenza A virus (IAV) infection by influencing inflammation and immune regulation, but the impact of the different iNKT functional subsets (iNKT1, iNKT2, and iNKT17) in these responses is unclear. We used genetically altered mouse strains with normal numbers of iNKT cells, but different iNKT subset representation (NKTWT and NKTET2) to analyze the impact of different iNKT functional subsets on IAV infection outcomes. We show that IAV-infected NKTET2 mice have reduced weight loss, diminished myeloid recruitment and activation, and a 40% reduction in lung-infected areas compared with controls. This was accompanied by lower expression of inflammatory mediators (Ifna, Isg15, Ifit1) and chemoattractants Ccl2 and Cxcl2, along with elevated levels of type III interferon (Ifnl3). scRNAseq analysis of iNKTs suggests that these changes are driven by quantitative differences in iNKT responses, which are predominantly type I in NKTWT mice but type 17 in NKTET2 mice. These differences correlate with higher levels of Il22b and Il1b in NKTET2 mice lungs. Altogether our results indicate that changes in iNKT subset representation impact the outcome of IAV infections by changing the character of the early immune response. - Source: PubMed
Publication date: 2026/03/21
Luczak JustynaMilek OliwiaCarter HannahSchafer Christopher MAinsua-Enrich ErolaGriffin Courtney TWalters Matthew SKovats SusanAlberola-Ila José - Canine infectious respiratory disease complex (CIRDC) causes contagious respiratory disease in dogs and encompasses several etiologic agents. Viral pathogens associated with CIRDC include canine adenovirus type 2 (CAV-2), canine distemper virus (CDV), canine herpesvirus-1 (CaHV-1) and canine influenza virus (CIV). Vaccine availability and efficacy vary and there are currently no antivirals available for treatment. Interferons (IFNs) are at the frontline of the immune defense against many viral infections and interferon lambda (IFNL) has shown to be a potent antiviral. We hypothesized that canine interferon lambda-3 (IFNL3) treatment of canine respiratory epithelial cells (ALI-CRECs) will reduce replication of kennel cough viruses. ALI-CRECs were isolated, cultured and characterized morphologically and immunologically prior to infection with CDV, CaHV-1, CIV and CAV-2. The value of canine IFNL3 treatment for reducing viral titers as well as induction of interferon responses were evaluated for each virus. Treatment of ALI-CRECs with IFNL3 induced the expression of interferon stimulated genes. In addition, prophylactic IFNL3 administration resulted in a reduction in viral DNA with CT value changes of up to 13 intracellularly and up to 9 extracellularly. In contrast, for CDV and CaHV-1 a reduction in viral RNA/DNA was observed only intracellularly with CT value changes of up to 11 and up to 4 respectively. Prophylactic IFNL3 treatment also significantly reduced viral titers 1.2 to 3 log-fold for CAV-2, 0.9-2.5 log-fold for CDV, and 1.1-1.7 log-fold for CaHV-1. No effect of IFNL3 was observed for CIV RNA and CIV viral titers. Coinciding with a reduction in viral replication, interferon stimulated genes were differentially expressed in interferon treated and infected cells when compared with controls. In conclusion, ALI-CRECs have shown to be excellent systems to study respiratory viruses and evaluate the potential antiviral effect of IFNL3. However further in-depth mechanistic studies are needed to fully understand how IFNL3 stimulates/modulates local immune responses to induce antiviral effects. Moreover, while this study highlights the potential antiviral efficacy of IFNL3 for several canine respiratory viruses, determination of safety, effective doses in vivo as well as therapeutic potential will have to be evaluated in dogs. - Source: PubMed
Publication date: 2026/05/03
Sharma SwatiBerríos-Vázquez GloriánBaldwin KennedyMaes RogerHussey Gisela Soboll