IL_29 (human) Singleplex MultiBead Kit
- Known as:
- IL_29 (H. sapiens) Singleplex MultiBead Kit
- Catalog number:
- ASA985-025
- Product Quantity:
- 96 Well
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- IL_29 (human) Singleplex MultiBead Kit
Related genes to: IL_29 (human) Singleplex MultiBead Kit
- Gene:
- IFNL1 NIH gene
- Name:
- interferon lambda 1
- Previous symbol:
- IL29
- Synonyms:
- IL-29
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-12-02
- Date modifiied:
- 2016-10-11
Related products to: IL_29 (human) Singleplex MultiBead Kit
Related articles to: IL_29 (human) Singleplex MultiBead Kit
- Type I and III interferons (IFNs) are among the first lines of defense against viral infection, yet they are generally only produced by a tiny fraction of infected cells. Here, we show that cellular heterogeneity in IFN-induction potential upon treatment with immunostimulatory RNA is not due to variability in sensing of stimuli but instead is shaped by heterogeneity in tonic cell signaling state. Using complementary single-cell approaches, we found that baseline variation in the expression of c-Jun N-terminal kinase (JNK) and activator protein (AP)-1 transcription factor families correlated with IFNL1 expression predisposition. We further show that drug-based inhibition of JNK signaling virtually eliminates the innate antiviral response to immunostimulatory RNA. Finally, we show that single-cell heterogeneity in IFN-induction potential is heritable and stably maintained over numerous generations. Together, our study emphasizes the influence of intrinsic variability in cell state on innate immune regulation and IFN-induction heterogeneity. - Source: PubMed
Publication date: 2026/07/16
Thayer Elizabeth AShipman GabrielaRivera-Cardona JoelMahajan TarunTeo Qi WenPaez J SebastianLederer JosephChen JieWu Nicholas CMaslov SergeiBrooke Christopher B - Eosinophil esophagitis (EoE) shares many epidemiologic and pathophysiologic characteristics with other allergic diseases, especially allergic asthma. Because rhinovirus (RV) infection is known to contribute to inflammation in allergic asthma, we sought to investigate whether RV might also contribute to esophageal inflammation in EoE through epithelial activation. In vitro cultures of primary esophageal epithelial cells and a human nontransformed immortalized esophageal epithelial cell line (EPC2-hTERT) grown submerged or at air-liquid interface were infected with RV-A1a or RV-A16. In addition, we added interleukin (IL)-13 to mimic EoE conditions. RV-binding receptors, RV replication, and interferon lambda-1 (IFNL1) response to infection were measured. RNA sequencing (RNA-seq) on RV-infected EPC2-hTERT cultures was performed for Gene Ontology analysis and compared with published RNA-seq data of esophageal biopsies from EoE patients. Both RV receptors were expressed by esophageal cells. After infection, we observed higher RV viral gene expression, indicative of active replication. IL-13 had little effect on replication in monolayers but was required in air-liquid interface for replication to occur. Interferon lambda-1 (IFNL1) messenger RNA was induced by RV-A1a in both cell types and IFNL1 protein was increased in IL-13-treated EPC2-hTERT monolayers. Gene Ontology analysis of our in vitro experimental model highlighted virus-induced processes and increased IFN activity. In addition, we found overlapping genes between our RNA-seq results of EPC2-hTERT cells and publicly available RNA-seq data from esophageal biopsies of patients with EoE versus healthy control donors. Our data suggest the possibility that viruses such as RV may contribute to esophageal inflammation and play an important role in the inception and/or persistence of EoE. - Source: PubMed
Fichtinger Paul SSonsalla Samuel GJohansson Mats WSamarasinghe Amali ELomeli Luis DMathur Sameer K - SARS-CoV-2 portrays a public health threat because severe progression of infections can lead to hospitalization. Severity is often characterized by a systemic inflammatory response in later stages, along with disbalance in cytokine production, multi-organ failure, or acute respiratory distress syndrome (ARDS). As severe infections can be challenging due to limited treatment windows for direct-acting antivirals, host-targets, e.g., the Raf/MEK/ERK signaling cascade, came into focus. Specifically, MEK1/2 has been suggested as a target for antiviral and anti-inflammatory therapy. A recent phase II clinical trial showed the efficacy of the MEK1/2 inhibitor zapnometinib (ZMN/ATR-002) in hospitalized COVID-19 patients. The anti-inflammatory action of ATR-002 was only studied on some candidate cytokines. - Source: PubMed
Publication date: 2026/05/29
Rodner FranziskaSchughart KlausLudwig StephanSchreiber André - Rift Valley fever virus (RVFV) is a mosquito-borne Phlebovirus and zoonotic pathogen affecting maternal-fetal health. Vertical transmission is linked to miscarriage and severe fetal outcomes, but mechanisms of placental pathogenesis remain unclear. We used first-trimester human trophoblast stem cells (hTSCs) to model infection at the maternal-fetal interface. Immunofluorescence, qRT-PCR, western blotting, and single-cell transcriptomics showed that hTSCs are highly susceptible to RVFV. Strand-specific viral transcriptomics confirmed the ambisense S segment and revealed preferential transcription of the M and S segments over L. RVFV induced G1 arrest, impairing trophoblast proliferation and differentiation, and drove widespread transcriptional reprogramming, including strong interferon lambda 1 () but modest type I interferon responses, and dysregulation of inflammatory and preeclampsia-associated genes such as and . Recombinant IFN-λ pretreatment reduced RVFV protein expression, highlighting hTSCs as a robust model and IFN-λ as a promising antiviral strategy. - Source: PubMed
Publication date: 2026/04/03
Gwon Yong-DaeHaider SandraKnöfler MartinBradley MatthewHenriksson JohanEvander Magnus - Glioblastoma (GBM) is an aggressive tumor with limited therapeutic options. Zika virus (ZIKV) has demonstrated activity against GBM; however, the cellular pathways behind this interaction remain unclear. We systematically reviewed open-access primary studies assessing differentially expressed genes (DEGs) in GBM models infected with wild-type or engineered ZIKV using transcriptomic approaches (inclusion criteria); reviews, restricted-access studies, commentaries, preprints, abstracts, and articles lacking data or not meeting these conditions were excluded (PROSPERO CRD420251077092). We performed a pathway analysis of reported DEGs. PubMed and Google Scholar were searched up to 5 March 2025; 139 records were identified and 5 met the eligibility criteria. Risk of bias was evaluated using an adapted ToxRTool for in vitro experiments and the SYRCLE RoB tool for in vivo models. Altogether, 4360 genes were reported as upregulated and 2072 as downregulated; 12 genes (, , , , , , , , , , , and ) were consistently upregulated, none were consistently downregulated. Pathway analysis of the studies providing complete DEG lists identified 23 commonly enriched pathways mostly related to interferon signaling. These findings may help guide future research in this field; nevertheless, methodological heterogeneity limits comparability, reinforcing the need for standardized protocols. Funding: ITpS, CNPq, and FAPEMIG. - Source: PubMed
Publication date: 2026/02/15
Menezes DiegoReis Clarisse RezendeMamede IzabelaGeddes Victor Emmanuel Vianade Souza Renan PedraAguiar Renato Santana