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R&D Systems human interferon λ1

Analysis of <t>interferon</t> (‐response) genes upon coronavirus infection and effects of <t>IFN‐λ1</t> supplementation on viral load. (a) Volcano plots depicting shared gene expression profiles of bronchial epithelial cell cultures infected with SARS‐CoV, SARS‐CoV‐2 or MERS‐CoV for (a) 24, (b) 48 hpi or (c) 72 hpi in comparison to HCoV‐229E and HCoV‐OC43; n = 4. Red dots indicate significantly upregulated genes, and blue dots indicate significantly downregulated genes. (d) Heatmap of the overlap of significantly changed genes during 24, 48 and 72 hpi infection with SARS‐CoV‐2, SARS‐CoV, MERS‐CoV or HCoV‐229E or HCoV‐OC43 and mock as uninfected control. (e) Gene set variation analysis (GSVA) was performed on interferon response genes after 24, 48 and 72 hpi ( n = 4) in highly pathogenic (orange) and low pathogenic (blue) coronavirus‐infected cultures. As HCoV‐OC43 infection was conducted at 33°C, SARS‐CoV‐2 infection at 33°C was included as control (pink). (f) IFN‐λ1 and (g) IFN‐α1 gene expression after 24, 48 and 72 hpi ( n = 4) in highly pathogenic (orange) and low pathogenic (blue) coronavirus‐infected cultures. The error bar indicates the standard deviation. Significant differences in increased gene expression over time of infection ( P < 0.05) are shown by the * symbol. Two‐way ANOVA followed by an unprotected Fisher's least significance difference test was conducted to test for significance. (h) ALI‐PBEC cultures were pretreated with 5 ng mL −1 interferon lambda (IFN‐λ1) for 60 min and subsequently infected with SARS‐CoV‐2 for 3 days with IFN‐λ1 present in the basal medium. Extracellular viral RNA copies are depicted in log scale. Data in h were analysed with a paired t ‐test and are depicted as mean ± SEM. n = 4 independent donors.

Human Interferon λ1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/interferon+lambda-1/Recombinant+Human+IL-29%2FIFN-lambda+1+Protein%2C+CF/pmc11017760-217-9-13
Average 92 stars, based on 11 article reviews

human interferon λ1 - by Bioz Stars, 2026-11

92/100 stars

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1) Product Images from "SARS ‐ C o V ‐2‐infected human airway epithelial cell cultures uniquely lack interferon and immediate early gene responses caused by other coronaviruses"

Article Title: SARS ‐ C o V ‐2‐infected human airway epithelial cell cultures uniquely lack interferon and immediate early gene responses caused by other coronaviruses

Journal: Clinical & Translational Immunology

doi: 10.1002/cti2.1503

Analysis of interferon (‐response) genes upon coronavirus infection and effects of IFN‐λ1 supplementation on viral load. (a) Volcano plots depicting shared gene expression profiles of bronchial epithelial cell cultures infected with SARS‐CoV, SARS‐CoV‐2 or MERS‐CoV for (a) 24, (b) 48 hpi or (c) 72 hpi in comparison to HCoV‐229E and HCoV‐OC43; n = 4. Red dots indicate significantly upregulated genes, and blue dots indicate significantly downregulated genes. (d) Heatmap of the overlap of significantly changed genes during 24, 48 and 72 hpi infection with SARS‐CoV‐2, SARS‐CoV, MERS‐CoV or HCoV‐229E or HCoV‐OC43 and mock as uninfected control. (e) Gene set variation analysis (GSVA) was performed on interferon response genes after 24, 48 and 72 hpi ( n = 4) in highly pathogenic (orange) and low pathogenic (blue) coronavirus‐infected cultures. As HCoV‐OC43 infection was conducted at 33°C, SARS‐CoV‐2 infection at 33°C was included as control (pink). (f) IFN‐λ1 and (g) IFN‐α1 gene expression after 24, 48 and 72 hpi ( n = 4) in highly pathogenic (orange) and low pathogenic (blue) coronavirus‐infected cultures. The error bar indicates the standard deviation. Significant differences in increased gene expression over time of infection ( P < 0.05) are shown by the * symbol. Two‐way ANOVA followed by an unprotected Fisher's least significance difference test was conducted to test for significance. (h) ALI‐PBEC cultures were pretreated with 5 ng mL −1 interferon lambda (IFN‐λ1) for 60 min and subsequently infected with SARS‐CoV‐2 for 3 days with IFN‐λ1 present in the basal medium. Extracellular viral RNA copies are depicted in log scale. Data in h were analysed with a paired t ‐test and are depicted as mean ± SEM. n = 4 independent donors.

Figure Legend Snippet: Analysis of interferon (‐response) genes upon coronavirus infection and effects of IFN‐λ1 supplementation on viral load. (a) Volcano plots depicting shared gene expression profiles of bronchial epithelial cell cultures infected with SARS‐CoV, SARS‐CoV‐2 or MERS‐CoV for (a) 24, (b) 48 hpi or (c) 72 hpi in comparison to HCoV‐229E and HCoV‐OC43; n = 4. Red dots indicate significantly upregulated genes, and blue dots indicate significantly downregulated genes. (d) Heatmap of the overlap of significantly changed genes during 24, 48 and 72 hpi infection with SARS‐CoV‐2, SARS‐CoV, MERS‐CoV or HCoV‐229E or HCoV‐OC43 and mock as uninfected control. (e) Gene set variation analysis (GSVA) was performed on interferon response genes after 24, 48 and 72 hpi ( n = 4) in highly pathogenic (orange) and low pathogenic (blue) coronavirus‐infected cultures. As HCoV‐OC43 infection was conducted at 33°C, SARS‐CoV‐2 infection at 33°C was included as control (pink). (f) IFN‐λ1 and (g) IFN‐α1 gene expression after 24, 48 and 72 hpi ( n = 4) in highly pathogenic (orange) and low pathogenic (blue) coronavirus‐infected cultures. The error bar indicates the standard deviation. Significant differences in increased gene expression over time of infection ( P < 0.05) are shown by the * symbol. Two‐way ANOVA followed by an unprotected Fisher's least significance difference test was conducted to test for significance. (h) ALI‐PBEC cultures were pretreated with 5 ng mL −1 interferon lambda (IFN‐λ1) for 60 min and subsequently infected with SARS‐CoV‐2 for 3 days with IFN‐λ1 present in the basal medium. Extracellular viral RNA copies are depicted in log scale. Data in h were analysed with a paired t ‐test and are depicted as mean ± SEM. n = 4 independent donors.

Techniques Used: Infection, Gene Expression, Comparison, Control, Standard Deviation

Recombinant:

Article Title: SARS ‐ C o V ‐2‐infected human airway epithelial cell cultures uniquely lack interferon and immediate early gene responses caused by other coronaviruses
Article Snippet: The potential cytotoxicity of the compounds was tested in parallel on uninfected cells in 96‐well plates using the CellTiter 96 Aqueous One Solution Cell Proliferation Assay (Promega). .. ALI‐PBEC were pretreated with 5 ng mL −1 recombinant human interferon λ1 (IFN‐λ1; R&D Systems, Minneapolis, USA) for 60 min, and further infected with SARS‐CoV‐2 (estimated MOI of 1) with the presence of IFN‐λ1 in the basal medium. ..

Article Title: HepG2 cells mount an effective antiviral interferon-lambda based innate immune response to hepatitis C virus infection
Article Snippet: For silencing, HepG2-HFL cells were transduced with pLKO.1 lentiviruses expressing short hairpin RNAs (shRNAs) with no target (SHC002; Sigma, St. Louis, MO) or targeting RIG-I (TRCN0000153712; Thermo Scientific, Lafayette, CO), MDA5 (Richard E. Randall, University of St. Andrews, United Kingdom), or IL28RA (#1 TRCN0000058990, #2 TRCN0000058991; Thermo Scientific). .. Interferon response assay was performed with IFN-λ 1 (recombinant human IL-29; R&D systems, Minneapolis, MN) and IFN; (human lymphoblastoid interferon alpha; BEI Resources, Manassas, VA). ..

Article Title: Type III interferon inhibits bladder cancer progression by reprogramming macrophage-mediated phagocytosis and orchestrating effective immune responses
Article Snippet: Resting Mφs were obtained by culturing 106/ml CD14+ monocytes for six days in RPMI 1640 containing 10% FBS with 25 ng/ml recombinant human M-CSF (PeproTech, USA). .. Mφs were polarized by stimulating them with 10 ng/ml recombinant human IFN-α (rh IFN-α, R&D Systems, USA) or 100 ng/ml recombinant human IFN-λ1 (rh IFN-λ1, R&D Systems, USA; Table S6) for either 6 or 12 h. Generations of bone marrow-derived Mφs To generate BMDMs, bone marrow cells were collected from femurs and tibias of 6–8-week-old C57BL/6J mice34. .. After lyzing the erythrocytes with RBC Lysis Buffer (CWBio, China), 1×106 cells/ml were seeded in 6-well plates.

Article Title: Type III interferon inhibits bladder cancer progression by reprogramming macrophage-mediated phagocytosis and orchestrating effective immune responses.
Article Snippet: .. D ow nloaded from 5Wang B, et al. J Immunother Cancer 2024;12:e007808. doi:10.1136/jitc-2023-007808 mL recombinant human IFN-α (rhIFN-α, R&D Systems, USA) or 100 ng/mL recombinant human IFN-λ1 (rhIFNλ1, R&D Systems, USA; online supplemental table 6) for either 6 or 12 hours. .. To generate bone marrow- derived Mφs (BMDMs), bone marrow cells were collected from femurs and tibias of C57BL/6J mice aged 6–8 weeks old.27 35 After lyzing the erythrocytes with RBC Lysis Buffer (CWBio, China), 1×106 cells/mL were seeded in 6- well plates.

Article Title: Role of interferons (IFNs) in the differentiation of T peripheral helper (Tph) cells.
Article Snippet: We reviewed the data of consecutive patients who visited Keio University Hospital from May 2015–December 2019, and were diagnosed with SLE, RA, p-SS, SSc, MCTD, VAS or IIM according to their respective classification criteria (19–25). .. Recombinant human (rh)-IL-12, and TGF-β1 were obtained from Peprotech (Cranbury, NJ). rh-IFN-α2a was purchased from PBL Assay Science (Piscataway, NJ). rh-IFN-λ1/IL-29, IFN-λ2/IL-28A and IFN-λ3/IL28B were obtained from R&D Systems (Minneapolis, MN). .. Anti-CD3 (OKT3) and anti-CD28 (CD28.2) monoclonal antibodies (mAbs) were obtained from eBioscience (San Diego, CA).

Article Title: Interferon-λ1 suppresses invasion and enhances autophagy in human osteosarcoma cell
Article Snippet: .. Recombinant Human IL-29/ IFN-λ1 (R&D Systems) was diluted in serum-free medium. ..

Infection:

Image Search Results

Journal: eLife

Article Title: Phospholipid scramblase 1 (PLSCR1) regulates interferon-lambda receptor 1 (IFN-λR1) and IFN-λ signaling in influenza A virus (IAV) infection

doi: 10.7554/eLife.104359

Figure Lengend Snippet: Wild-type (WT) and Plscr1 -/- mice were exposed to sublethal (300 pfu) influenza A virus (IAV) (WSN) infection. ( A ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( B ) Differential cell counts in BAL. ( C ) Representative lung sections stained with Hematoxylin and Eosin (H&E). Scale bars represent 3 mm (main) and 200 μm (inlays). ( D ) Whole lungs were analyzed for Ifna , Ifnb , Ifng, and Ifnl RNA by qRT-PCR. ( E ) Tnf-α and Ifn-λ concentrations in BAL by ELISA. Data are expressed as mean ± SEM of n=3–14 mice/group. All data were pooled from three independent experiments and described biological replicates. * p <0.05, ** p <0.01. dpi, days post-infection.

Article Snippet: In control Calu-3 groups, cells were first incubated with 1 μg/mL of anti-human interferon lambda receptor 1 neutralizing antibody (PBL Assay Science, cat #21885–1, clone #MMHLR-1) for 1 hr, and then treated with IFN-λ.

Techniques: Virus, Infection, Staining, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Wild-type (WT) and Plscr1-/- mice were intranasally given 2.5 μg/g of body weight of poly(I:C) (HMW) constitutively for 6 days and sacrificed on day 7. ( A ) Scheme of experiment. ( B ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( C ) Differential cell counts in BAL. ( D, F, G ) Whole lungs were analyzed for Ifna, Ifnb, Ifng, Ifnl ( D ); Plscr1 ( F ); and Ifnlr1 ( G ) RNA by qRT-PCR. ( E ) Representative lung sections stained with Hematoxylin and Eosin (H&E). Scale bars represent 3 mm (main) and 200 μm (inlays). Data are expressed as mean ± SEM of n=5–12 mice/group. All data were pooled from three independent experiments and described biological replicates. ns, not significant, *p<0.05, ***p<0.001.

Journal: eLife

Article Title: Phospholipid scramblase 1 (PLSCR1) regulates interferon-lambda receptor 1 (IFN-λR1) and IFN-λ signaling in influenza A virus (IAV) infection

doi: 10.7554/eLife.104359

Figure Lengend Snippet: Wild-type (WT) and Plscr1-/- mice were intranasally given 2.5 μg/g of body weight of poly(I:C) (HMW) constitutively for 6 days and sacrificed on day 7. ( A ) Scheme of experiment. ( B ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( C ) Differential cell counts in BAL. ( D, F, G ) Whole lungs were analyzed for Ifna, Ifnb, Ifng, Ifnl ( D ); Plscr1 ( F ); and Ifnlr1 ( G ) RNA by qRT-PCR. ( E ) Representative lung sections stained with Hematoxylin and Eosin (H&E). Scale bars represent 3 mm (main) and 200 μm (inlays). Data are expressed as mean ± SEM of n=5–12 mice/group. All data were pooled from three independent experiments and described biological replicates. ns, not significant, *p<0.05, ***p<0.001.

Techniques: Quantitative RT-PCR, Staining

Plscr1 floxStop and Plscr1 floxStop ;Foxj1-Cre + mice were exposed to sublethal (300 pfu) influenza A virus (IAV) (WSN) infection and sacrificed at 3 dpi. ( A ) Schematic representation of the experimental design of ciliated epithelial cell conditional Plscr1 KI mice. ( B ) Validation of Plscr1 overexpression in lungs of Plscr1 floxStop ;Foxj1-Cre + mice by qRT-PCR. ( C ) Representative immunofluorescent staining for Plscr1, Ifn-λr1, and Foxj1 in lungs. Scale bars represent 50 μm (main) and 10 μm (inlays).( D ) Mean relative weight of mice. ( E ) Viral RNA load in the lungs was assessed by quantifying M gene by qRT-PCR. ( F ) Infectious viral titer in the lungs was assessed by plaque assays. ( G ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( H ) Neutrophil percentages in BAL. ( I ) Whole lungs were analyzed for Ifnlr1 RNA by qRT-PCR and Ifn-λr1 protein by western blot. ( J ) Whole lungs were analyzed for Ifna , Ifnb , Ifng , and Ifnl RNA by qRT-PCR. ( K ) Model depicting proposed mechanism of PLSCR1-regulated IFN-λ signaling. Data are expressed as mean ± SEM of n=3–10 mice/group. All data were pooled from three independent experiments and described biological replicates. ns, not significant, * p <0.05, ** p <0.01, *** p <0.001. dpi, days post-infection. Figure 8—source data 1. PDF file containing original membrane for , indicating the relevant bands and treatments. The membrane was cut just under 50 kDa marker after transfer. The top part was incubated with α-Ifn-λr1 antibody and the bottom part was incubated with α-β-actin antibody. They were then incubated with corresponding secondary antibodies separately. The exposure time was adjusted to visualize Ifn-λr1 (top) or β-actin (middle). A colorimetric photo was taken to visualize the molecular weight markers (bottom). Lanes 2 and 3 were from an unrelated experiment. Figure 8—source data 2. Original membrane corresponding to .

Journal: eLife

Article Title: Phospholipid scramblase 1 (PLSCR1) regulates interferon-lambda receptor 1 (IFN-λR1) and IFN-λ signaling in influenza A virus (IAV) infection

doi: 10.7554/eLife.104359

Figure Lengend Snippet: Plscr1 floxStop and Plscr1 floxStop ;Foxj1-Cre + mice were exposed to sublethal (300 pfu) influenza A virus (IAV) (WSN) infection and sacrificed at 3 dpi. ( A ) Schematic representation of the experimental design of ciliated epithelial cell conditional Plscr1 KI mice. ( B ) Validation of Plscr1 overexpression in lungs of Plscr1 floxStop ;Foxj1-Cre + mice by qRT-PCR. ( C ) Representative immunofluorescent staining for Plscr1, Ifn-λr1, and Foxj1 in lungs. Scale bars represent 50 μm (main) and 10 μm (inlays).( D ) Mean relative weight of mice. ( E ) Viral RNA load in the lungs was assessed by quantifying M gene by qRT-PCR. ( F ) Infectious viral titer in the lungs was assessed by plaque assays. ( G ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( H ) Neutrophil percentages in BAL. ( I ) Whole lungs were analyzed for Ifnlr1 RNA by qRT-PCR and Ifn-λr1 protein by western blot. ( J ) Whole lungs were analyzed for Ifna , Ifnb , Ifng , and Ifnl RNA by qRT-PCR. ( K ) Model depicting proposed mechanism of PLSCR1-regulated IFN-λ signaling. Data are expressed as mean ± SEM of n=3–10 mice/group. All data were pooled from three independent experiments and described biological replicates. ns, not significant, * p <0.05, ** p <0.01, *** p <0.001. dpi, days post-infection. Figure 8—source data 1. PDF file containing original membrane for , indicating the relevant bands and treatments. The membrane was cut just under 50 kDa marker after transfer. The top part was incubated with α-Ifn-λr1 antibody and the bottom part was incubated with α-β-actin antibody. They were then incubated with corresponding secondary antibodies separately. The exposure time was adjusted to visualize Ifn-λr1 (top) or β-actin (middle). A colorimetric photo was taken to visualize the molecular weight markers (bottom). Lanes 2 and 3 were from an unrelated experiment. Figure 8—source data 2. Original membrane corresponding to .

Techniques: Virus, Infection, Biomarker Discovery, Over Expression, Quantitative RT-PCR, Staining, Western Blot, Membrane, Marker, Incubation, Molecular Weight

Plscr1 floxStop and Plscr1 floxStop ;Lyz2-Cre + mice were exposed to sublethal (300 pfu) influenza A virus (IAV) (WSN) infection. ( A ) Validation of Plscr1 overexpression in lungs of Plscr1 floxStop ;Lyz2-Cre + mice by qRT-PCR. ( B ) Mean relative weight of mice. ( C ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( D ) Differential cell counts in BAL. ( E ) Viral RNA load in the lungs was assessed by quantifying M gene by qRT-PCR. ( F ) Representative lung sections stained with Hematoxylin and Eosin (H&E). Scale bars represent 3 mm (main) and 200 μm (inlays). ( G–I ) Whole lungs were analyzed for Ifna , Ifnb , Ifng , Ifnl ( G ); Ifnlr1 ( H ); and Plscr1 ( I ) RNA by qRT-PCR. Data are expressed as mean ± SEM of n=15–16 mice/group for weight loss. For the rest analysis, n=3–7 mice/group. All data were pooled from three independent experiments and described biological replicates. ns, not significant, ** p <0.01. dpi, days post-infection.

Journal: eLife

Article Title: Phospholipid scramblase 1 (PLSCR1) regulates interferon-lambda receptor 1 (IFN-λR1) and IFN-λ signaling in influenza A virus (IAV) infection

doi: 10.7554/eLife.104359

Figure Lengend Snippet: Plscr1 floxStop and Plscr1 floxStop ;Lyz2-Cre + mice were exposed to sublethal (300 pfu) influenza A virus (IAV) (WSN) infection. ( A ) Validation of Plscr1 overexpression in lungs of Plscr1 floxStop ;Lyz2-Cre + mice by qRT-PCR. ( B ) Mean relative weight of mice. ( C ) Total Bronchoalveolar lavage (BAL) leukocyte numbers. ( D ) Differential cell counts in BAL. ( E ) Viral RNA load in the lungs was assessed by quantifying M gene by qRT-PCR. ( F ) Representative lung sections stained with Hematoxylin and Eosin (H&E). Scale bars represent 3 mm (main) and 200 μm (inlays). ( G–I ) Whole lungs were analyzed for Ifna , Ifnb , Ifng , Ifnl ( G ); Ifnlr1 ( H ); and Plscr1 ( I ) RNA by qRT-PCR. Data are expressed as mean ± SEM of n=15–16 mice/group for weight loss. For the rest analysis, n=3–7 mice/group. All data were pooled from three independent experiments and described biological replicates. ns, not significant, ** p <0.01. dpi, days post-infection.

Techniques: Virus, Infection, Biomarker Discovery, Over Expression, Quantitative RT-PCR, Staining

Influenza infection is usually detected by intracellular pattern recognition receptors (PRRs) such as TLR 3 and 7, RIG-I, and MDA5. These PRRs activate the expression of IFNL in early infection stage through IRF-3 and NK-κB-controlled transcriptions. IFN-λ secreted by the infected cells interacts with IL-10R2 and IFN-λR1 on neighboring cell surfaces, which results in activation of expression of various IFN-stimulated genes, including PLSCR1 . In ciliated airway epithelial cells, PLSCR1 can further enhance the transcription of IFNLR1 by directly binding to its promoter region as a transcriptional factor, or interact with IFN-λR1 on the cell membrane.

Journal: eLife

Article Title: Phospholipid scramblase 1 (PLSCR1) regulates interferon-lambda receptor 1 (IFN-λR1) and IFN-λ signaling in influenza A virus (IAV) infection

doi: 10.7554/eLife.104359

Figure Lengend Snippet: Influenza infection is usually detected by intracellular pattern recognition receptors (PRRs) such as TLR 3 and 7, RIG-I, and MDA5. These PRRs activate the expression of IFNL in early infection stage through IRF-3 and NK-κB-controlled transcriptions. IFN-λ secreted by the infected cells interacts with IL-10R2 and IFN-λR1 on neighboring cell surfaces, which results in activation of expression of various IFN-stimulated genes, including PLSCR1 . In ciliated airway epithelial cells, PLSCR1 can further enhance the transcription of IFNLR1 by directly binding to its promoter region as a transcriptional factor, or interact with IFN-λR1 on the cell membrane.

Techniques: Infection, Expressing, Activation Assay, Binding Assay, Membrane

(A) Duolink PLA was performed to examine interactions of FLAG-Iso1 and FLAG-Iso2 with IL10RB after IFNL3 stimulation (15min). Yellow puncta represent complex formation; nuclei were counterstained with DAPI (blue) and imaged by scanning confocal microscopy. Scale bar, 20µm. (B) Quantitation of mean puncta per cell showing comparable ability of FLAG-Iso1 and -Iso2 to form ligand-induced complexes with IL10RB. Three images per condition were analyzed, mean ± SEM shown. n=43 cells per image. ( C ) Representative brightfield and fluorescent images of dox-induced FLAG-Iso1 and –Iso2 cells pre-incubated with anti-FLAG antibody at 4°C, then shifted to 37°C in the presence or absence of IFNL3 showing redistribution of FLAG-specific fluorescent signal (green) over time. Images selected at each time point represent cells with comparable peripheral FLAG-specific fluorescent signal that corresponded with the mean observed for the total population. (D) Quantitation of FLAG-specific signal at the cell surface, normalized to the respective time point zero. n= 5000 live events, mean ± SEM shown. *p≤ 0.05, comparing FLAG-Iso1 to –Iso2 at each timepoint.

Journal: bioRxiv

Article Title: Mechanisms of Differential Signal Transduction by IFNLR1 Variants

doi: 10.1101/2025.10.03.677101

Figure Lengend Snippet: (A) Duolink PLA was performed to examine interactions of FLAG-Iso1 and FLAG-Iso2 with IL10RB after IFNL3 stimulation (15min). Yellow puncta represent complex formation; nuclei were counterstained with DAPI (blue) and imaged by scanning confocal microscopy. Scale bar, 20µm. (B) Quantitation of mean puncta per cell showing comparable ability of FLAG-Iso1 and -Iso2 to form ligand-induced complexes with IL10RB. Three images per condition were analyzed, mean ± SEM shown. n=43 cells per image. ( C ) Representative brightfield and fluorescent images of dox-induced FLAG-Iso1 and –Iso2 cells pre-incubated with anti-FLAG antibody at 4°C, then shifted to 37°C in the presence or absence of IFNL3 showing redistribution of FLAG-specific fluorescent signal (green) over time. Images selected at each time point represent cells with comparable peripheral FLAG-specific fluorescent signal that corresponded with the mean observed for the total population. (D) Quantitation of FLAG-specific signal at the cell surface, normalized to the respective time point zero. n= 5000 live events, mean ± SEM shown. *p≤ 0.05, comparing FLAG-Iso1 to –Iso2 at each timepoint.

Article Snippet: WT- and IFNLR1 -KO-iHeps harboring FLAG-Iso1, FLAG-Iso2, and EV constructs were +/-dox-induced (100ng/ml, 24h) then mock, IFNL3 (100ng/ml), or IFNA2 (100ng/ml, PBL Assay Science) stimulated at 37°C for 15min, then collected and lysed on ice in RIPA buffer (ThermoFisher) supplemented with protease and phosphatase inhibitors (Pierce).

Techniques: Confocal Microscopy, Quantitation Assay, Incubation

Western blot analysis of whole cell lysates from ( A ) WT iHeps and ( B ) IFNLR1 -KO iHeps +/-dox-induced for 24h then treated +/-IFNL3 or IFNA2 for 15min. GAPDH served as an indicator of equivalent protein loading per lane. The ratio of phosphorylated to total protein for ( C ) dox-uninduced WT iHeps and ( D ) dox-induced IFNLR1 -KO iHeps +/-IFNL3 is shown as a percentage, based on integrated band intensity determined in ImageJ.

Journal: bioRxiv

Article Title: Mechanisms of Differential Signal Transduction by IFNLR1 Variants

doi: 10.1101/2025.10.03.677101

Figure Lengend Snippet: Western blot analysis of whole cell lysates from ( A ) WT iHeps and ( B ) IFNLR1 -KO iHeps +/-dox-induced for 24h then treated +/-IFNL3 or IFNA2 for 15min. GAPDH served as an indicator of equivalent protein loading per lane. The ratio of phosphorylated to total protein for ( C ) dox-uninduced WT iHeps and ( D ) dox-induced IFNLR1 -KO iHeps +/-IFNL3 is shown as a percentage, based on integrated band intensity determined in ImageJ.

Techniques: Western Blot

Shown are MX1 and CXCL10 expression in iHeps pre-treated with JAK1-upadacitinib; IC 50 47nM) or TYK2-(deucravacitinib; IC 50 0.2nM) inhibitors prior to IFNL3 stimulation (100ng/ml, 24h) relative to mock-treated cells. ( A ) Comparison of MX1 expression in WT-Iso1 (+/-dox) and KO-Iso1 (+dox) iHep lines and ( B ) WT-Iso2 (+/-dox) and KO-Iso2 (+dox) iHep lines. ( C ) Comparison of MX1 expression in WT-Iso1 and WT-Iso2 iHep lines (-dox) and ( D ) KO-Iso1 and KO-Iso2 iHep lines (+dox). ( E ) Comparison of CXCL10 expression in WT-Iso1 (+/-dox) and KO-Iso1 (+dox) iHeps. Biological replicates were assayed in technical duplicate and mean ± SEM is shown relative to GAPDH . Results are representative of two independent experiments. Percent gene expression was calculated relative to respective mock treated samples. *, +, and _ indicate p≤ 0.05 by Student’s t-test.

Journal: bioRxiv

Article Title: Mechanisms of Differential Signal Transduction by IFNLR1 Variants

doi: 10.1101/2025.10.03.677101

Figure Lengend Snippet: Shown are MX1 and CXCL10 expression in iHeps pre-treated with JAK1-upadacitinib; IC 50 47nM) or TYK2-(deucravacitinib; IC 50 0.2nM) inhibitors prior to IFNL3 stimulation (100ng/ml, 24h) relative to mock-treated cells. ( A ) Comparison of MX1 expression in WT-Iso1 (+/-dox) and KO-Iso1 (+dox) iHep lines and ( B ) WT-Iso2 (+/-dox) and KO-Iso2 (+dox) iHep lines. ( C ) Comparison of MX1 expression in WT-Iso1 and WT-Iso2 iHep lines (-dox) and ( D ) KO-Iso1 and KO-Iso2 iHep lines (+dox). ( E ) Comparison of CXCL10 expression in WT-Iso1 (+/-dox) and KO-Iso1 (+dox) iHeps. Biological replicates were assayed in technical duplicate and mean ± SEM is shown relative to GAPDH . Results are representative of two independent experiments. Percent gene expression was calculated relative to respective mock treated samples. *, +, and _ indicate p≤ 0.05 by Student’s t-test.

Techniques: Expressing, Comparison, Gene Expression

Top pathways up-regulated by IFNL3 treatment in dox-uninduced WT-iHeps expressing FLAG-Iso1 ( A ) or FLAG-Iso2 ( B ) relative to similarly treated WT-EV iHeps. Pathways with at least 10 genes identified in the dataset represented within the indicated pathway are shown. Pathways identified in both datasets are indicated in red, with the number of genes from the dataset represented within each individual pathway indicated.

Journal: bioRxiv

Article Title: Mechanisms of Differential Signal Transduction by IFNLR1 Variants

doi: 10.1101/2025.10.03.677101

Figure Lengend Snippet: Top pathways up-regulated by IFNL3 treatment in dox-uninduced WT-iHeps expressing FLAG-Iso1 ( A ) or FLAG-Iso2 ( B ) relative to similarly treated WT-EV iHeps. Pathways with at least 10 genes identified in the dataset represented within the indicated pathway are shown. Pathways identified in both datasets are indicated in red, with the number of genes from the dataset represented within each individual pathway indicated.

Techniques: Expressing

Heat map of RNA-seq data showing column-normalized expression for the 35 IFNL3-induced DEGs identified in the “Interferon alpha beta signaling” pathway in WT-iHeps expressing FLAG-Iso1 relative to EV (-dox, + IFNL3) shown in ( A ) WT and ( B ) KO iHep samples with dox and IFNL3 treatment as indicated. Rows depict individual biological duplicate samples clustered by cell line and treatment; red indicates higher expression and blue represents lower expression ( C-D ) Relative expression of select genes ( MX1 , IFITM1 , IFITM3 ) evaluated by qRT-PCR relative to GAPDH in WT ( C ) and KO ( D ) iHeps showed correlation with RNA-seq data. Data are representative of two biological replicates assayed in technical duplicates relative to GAPDH . Mean ± SEM, *p≤0.05 by Student’s t-test.

Journal: bioRxiv

Article Title: Mechanisms of Differential Signal Transduction by IFNLR1 Variants

doi: 10.1101/2025.10.03.677101

Figure Lengend Snippet: Heat map of RNA-seq data showing column-normalized expression for the 35 IFNL3-induced DEGs identified in the “Interferon alpha beta signaling” pathway in WT-iHeps expressing FLAG-Iso1 relative to EV (-dox, + IFNL3) shown in ( A ) WT and ( B ) KO iHep samples with dox and IFNL3 treatment as indicated. Rows depict individual biological duplicate samples clustered by cell line and treatment; red indicates higher expression and blue represents lower expression ( C-D ) Relative expression of select genes ( MX1 , IFITM1 , IFITM3 ) evaluated by qRT-PCR relative to GAPDH in WT ( C ) and KO ( D ) iHeps showed correlation with RNA-seq data. Data are representative of two biological replicates assayed in technical duplicates relative to GAPDH . Mean ± SEM, *p≤0.05 by Student’s t-test.

Techniques: RNA Sequencing, Expressing, Quantitative RT-PCR

( A ) Model depicting the mechanisms of distinct signaling outcomes imparted by ternary complexes composed of IFNL3, IL10RB and either IFNLR1 variant 1 or 2. Greater arrow width indicates higher association and/or phosphorylation (JAK1, STAT1, STAT2), greater internalization of receptor complexes, or higher induction of gene expression. IFNLR1 variant 1 containing heterodimers are depicted to have greater stability of JAK1 and/or pJAK1 binding and to be more prone to internalization than IFNLR1 variant 2 containing heterodimers. This correlates with variant 1 mediating more efficient phosphorylation of STAT1 and STAT2 and supporting higher expression of antiviral ISGs and de novo expression of proinflammatory ISGs compared to variant 2. ( B ) Model depicting assemblage of multimeric clusters containing multiple heterodimers of IFNL3-bound IFNLR1 variants in complex with IL10RB. In this model, proximity of JAK1 molecules bound to the cytoplasmic domains of IFNLR1 variants 1 and 2 could participate in TYK2-independent transphosphorylation. The relative abundance of IFNLR1 variants within multimeric complexes would influence the nature of receptor internalization, STAT phosphorylation, and downstream gene expression. The TYK2 dependence of signaling differs for antiviral vs. proinflammatory ISG expression and has a complex relationship with the relative abundance of IFNLR1 variants. Soluble variant 3, not studied in these experiments, is included in the model for consideration. Created in BioRender. Novotny, L. (2025) https://BioRender.com/24aqcgc .

Journal: bioRxiv

Article Title: Mechanisms of Differential Signal Transduction by IFNLR1 Variants

doi: 10.1101/2025.10.03.677101

Figure Lengend Snippet: ( A ) Model depicting the mechanisms of distinct signaling outcomes imparted by ternary complexes composed of IFNL3, IL10RB and either IFNLR1 variant 1 or 2. Greater arrow width indicates higher association and/or phosphorylation (JAK1, STAT1, STAT2), greater internalization of receptor complexes, or higher induction of gene expression. IFNLR1 variant 1 containing heterodimers are depicted to have greater stability of JAK1 and/or pJAK1 binding and to be more prone to internalization than IFNLR1 variant 2 containing heterodimers. This correlates with variant 1 mediating more efficient phosphorylation of STAT1 and STAT2 and supporting higher expression of antiviral ISGs and de novo expression of proinflammatory ISGs compared to variant 2. ( B ) Model depicting assemblage of multimeric clusters containing multiple heterodimers of IFNL3-bound IFNLR1 variants in complex with IL10RB. In this model, proximity of JAK1 molecules bound to the cytoplasmic domains of IFNLR1 variants 1 and 2 could participate in TYK2-independent transphosphorylation. The relative abundance of IFNLR1 variants within multimeric complexes would influence the nature of receptor internalization, STAT phosphorylation, and downstream gene expression. The TYK2 dependence of signaling differs for antiviral vs. proinflammatory ISG expression and has a complex relationship with the relative abundance of IFNLR1 variants. Soluble variant 3, not studied in these experiments, is included in the model for consideration. Created in BioRender. Novotny, L. (2025) https://BioRender.com/24aqcgc .

Techniques: Variant Assay, Phospho-proteomics, Gene Expression, Binding Assay, Expressing

(A) IFNβ and (B) IFNλ3 proteins detected in top channel washes recovered at 4 days post-infection. (n=5 independent experiments with 5 different organoid lines. Each dot color represents an organoid line. Median +/- interquartile range are plotted and Kruskal-Wallis tests are used for addressing statistically significant differences).

Journal: bioRxiv

Article Title: Modeling viral and bacterial infections in human lung organotypic systems reveals strain specific host responses

doi: 10.1101/2025.03.31.644992

Figure Lengend Snippet: (A) IFNβ and (B) IFNλ3 proteins detected in top channel washes recovered at 4 days post-infection. (n=5 independent experiments with 5 different organoid lines. Each dot color represents an organoid line. Median +/- interquartile range are plotted and Kruskal-Wallis tests are used for addressing statistically significant differences).

Article Snippet: For the IFNλ3 assay, the 21730-1 IgG1, kappa, mouse monoclonal antibody (PBL Assay Science) was used as a capture antibody after coating on paramagnetic beads (0.3 mg.mL -1 ), the MAB52591R IgG2a, mouse monoclonal antibody (R&D Systems, Minneapolis, MN, USA) was biotinylated (biotin/antibody ratio = 60/1) and used as the detector antibody at a concentration of 0.3 μg.mL -1 , and the 5259-IL-025/CF recombinant human IFNλ3 protein (R&D Systems) was used as calibrator.

Techniques: Infection

Review

human interferon λ1 (R&D Systems)

Structured Review

Images

1) Product Images from "SARS ‐ C o V ‐2‐infected human airway epithelial cell cultures uniquely lack interferon and immediate early gene responses caused by other coronaviruses"

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