MAGNETIC STIRRER WITH LIGHT 2L
- Known as:
- MAGNETIC STIRRER LIGHT 2L
- Catalog number:
- ANS-014
- Category:
- -
- Supplier:
- SBS
- Gene target:
- MAGNETIC STIRRER WITH LIGHT 2L
Related genes to: MAGNETIC STIRRER WITH LIGHT 2L
- Gene:
- TNFRSF14 NIH gene
- Name:
- TNF receptor superfamily member 14
- Previous symbol:
- -
- Synonyms:
- HVEM, ATAR, TR2, LIGHTR, HVEA, CD270
- Chromosome:
- 1p36.32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2016-06-28
- Gene:
- TNFSF14 NIH gene
- Name:
- TNF superfamily member 14
- Previous symbol:
- -
- Synonyms:
- LIGHT, LTg, HVEM-L, CD258
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: MAGNETIC STIRRER WITH LIGHT 2L
"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555(for isolation and cultivation of Listeria from Henry’s light.)1 Magnetic Covered 100 Microtube Box1 Magnetic Covered 100 Microtube Box1-Channel S.S Adaptor (40mm), Light Blue1-Channel S.S Adaptor (80mm), Light Blue1-Channel Tip Adaptor with Tip Ejector, Light Blue1-Channel Tip Adaptor, Light Blue1-Step™ Accurate-Beads, Avidin-Coated Beads, Non-Magnetic Density Perturbation Method for Cell Sep.10 _SSRL Cassette Kits; contains sample storage cassette, 96 copper magnetic sample pins, a loading guide tool, a magnetic loading and testing wand, a dewar canister, a styrofoam spacer, a teflon supp Related articles to: MAGNETIC STIRRER WITH LIGHT 2L
- Somatic mutations can rewire tumor-immune interactions to favor cancer progression. Here, we define the functional impact of missense mutations in Herpesvirus entry mediator (HVEM, TNFRSF14), a receptor frequently altered in lymphoma and melanoma. - Source: PubMed
Publication date: 2026/09/11
Lin Wai WaiHuang SarahBalmert OliviaBjordahl RyanWare Brian CMoshayedi ArefNguyen JenniferWare Carl FŠedý John R - Studies with a candidate vaccine deleted in glycoprotein D (ΔgD-2) for herpes simplex virus (HSV) prevention uncovered a role for herpes virus entry mediator (HVEM) in mediating antibody-dependent cell-mediated killing (ADCK) of virally infected cells. Antibodies elicited by ΔgD-2 passively protect WT but not Fc γ receptor (FcγR) or HVEM knockout (KO) mice. The goals of this study were to identify which cells mediate ADCK and the role of HVEM signaling. Using HVEM ligand and conditional cell-type-specific HVEM-KO mice combined with in vitro mouse and human cytolytic assays, we demonstrate that ADCK of HSV-infected cells is mediated primarily by neutrophils and requires their expression of HVEM and its ligand, LIGHT. Cytolysis is not associated with granzyme and perforin production but occurs by a trogocytosis-like pathway. Pharmacological inhibition of myosin light-chain kinase (MLCK), which mediates trogocytosis, inhibits cytolysis. Similar results were obtained when human neutrophils were cocultured with HSV-infected cells opsonized with ADCK-containing human immune serum or with breast cancer cells treated with an anti-HER2 trogocytosis mediating antibody. Killing was significantly reduced when an MLCK inhibitor or blocking antibodies to CD16a, HVEM, or LIGHT were added. Together, these results define a mechanism of HVEM-enhanced FcγR-mediated neutrophil-dependent ADCK of targets cells. - Source: PubMed
Publication date: 2026/06/04
Gromisch Matthew SKuraoka MasayukiWare Carl FAlmo Steven CHerold Betsy C - Immune checkpoint blockade (ICB) targeting PD-1/PD-L1 axis has transformed breast cancer treatment, yet how therapy reshapes the tumor microenvironment (TME) through cell-cell communication (CCC) remains unclear. Existing CCC inference methods relying on correlations have difficulty distinguishing genuine signaling from confounded associations. Here, we present a causal inference framework that uses single-cell data and leverages treatment as an instrumental variable to identify genuine CCC networks, referred to as scIVCCC, which infers causal signal transduction across cell types. Applying scIVCCC to single-cell RNA-seq data from 31 breast cancer patients before and after anti-PD-1 therapy, we constructed causal CCC networks linking exhausted T cells to tumor-associated macrophages (TAMs). Our analysis reveals a dual role of T cell-macrophage crosstalk: CD4+ and CD8+ exhausted T cells drive anti-tumor M1-like TAMs activation via TNF-TNFRSF1A, TNFSF14-LTBR, and ICAM1-ITGAL/ITGB2. Conversely, they also induce immunosuppressive M2-like polarization through pathways such as TNF-TNFRSF1B (TNFR2), TNFSF14-TNFRSF14 (HVEM), and RPS19-C5AR1, which likely contribute to therapeutic resistance. Our causal modeling suggests that receptors within these networks, such as C5AR1, TNFR2, and CSF1R, may serve as potential candidates for combination therapies to enhance anti-PD-1 efficacy. Collectively, these findings demonstrate that scIVCCC offers a robust framework for dissecting treatment-induced CCC dynamics and prioritizing actionable targets for clinical translation. - Source: PubMed
Qiu AodongZhang HanRamsey Joseph DAndrews BryanSun BoyangRen ShuangxiaLu MengyaoZhang KunCooper Gregory FLu BinfengChen LujiaLu Xinghua - The pathogenesis of psoriasis is associated with abnormalities in immune pathways. HVEM is known as a receptor of LIGHT (homologous to lymphotoxins, inducible, and competes with HSV glycoprotein D), which is a newly identified member of the TNF superfamily. The expression of HVEM and LTBR (another LIGHT receptor) has been found to be increased in the skin of psoriasis patients. This indicates the potential role of LIGHT and its receptors in the pathogenesis of psoriasis. Therefore, the objective of this study was to examine the effect of LIGHT on keratinocyte proliferation and its therapeutic potential in the treatment of psoriasis. - Source: PubMed
Ye Cheng-BinFei Cheng-WenCao TingZhou Xu-YangZou Ying - Alveolar macrophages (AMs) help defend the lungs against infection, but during pneumonia many alveolar macrophages die. In this issue of the JCI, Malainou et al. explored the mechanism underpinning AM death during viral pneumonia and its effect on the outcomes of bacterial superinfection, a secondary infection that occurs before the first infection is cleared. In mouse models of influenza A infection, recruited neutrophils secreted TNF superfamily member 14 (TNFSF14), and AMs increased expression of the TNFSF14 receptors TNFSFR14 and type I transmembrane lymphotoxin β receptor (LTβR). TNFSF14 signaling via the LTβR was sufficient to cause AM apoptosis. TNFSF14 deficiency or blockade preserved AMs during influenza infection and diminished bacterial burdens and mouse mortality during pneumococcal superinfection. The adoptive transfer of AMs decreased the severity of pneumococcal superinfections, if those AMs lacked the LTβR. Thus, preserving AMs by interrupting TNFRSF14-LTβR interactions can make virus-infected lungs less susceptible to severe bacterial superinfection. - Source: PubMed
Publication date: 2026/01/16
Armstrong Elise MrMizgerd Joseph P