Ask about this productRelated genes to: LIGHT antibody
- 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: LIGHT antibody
Related articles to: LIGHT antibody
- 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 - To elucidate the mechanism through which tumor-associated neutrophil extracellular traps (NETs) contribute to the progression of colorectal cancer (CRC), characterize cellular populations within the CRC tumor microenvironment (TME), and identify potential therapeutic targets. - Source: PubMed
Publication date: 2025/11/11
Ying YaoWang HaochengWang YueHuang JunpengWu ZiyingQiu BowenChen HungchenLong MeitingMo KeCui Chunhui - T cells are important targets for therapeutic intervention in many diseases. Modifying T cell activation via immune checkpoints plays a central role in such approaches. The HVEM/LIGHT complex is one of the stimulatory immune checkpoints involved in T cell activation, and binding of these proteins results in proliferation and development of effector functions of T cells. In patients suffering from autoimmune diseases and in transplant recipients it is desirable to suppress immune responses. This could be achieved by blocking the HVEM and LIGHT interactions. Our studies concern blockage of the formation of the HVEM/LIGHT complex using peptides. To design the inhibitors of this interactions, we relied on the amino acid sequence and the structure of the LIGHT-binding fragments of HVEM. We measured the affinity of designed peptides to LIGHT using SpS technique and tested their ability to inhibit the formation of the HVEM/LIGHT complex using ELISA and cellular studies. That led to the identification of two peptides, namely CRD2e_K54E and CRD2(39-73)e that strongly bind to LIGHT and possess blocking capacities towards HVEM/LIGHT complex formation. Obtained data indicate that HVEM-derived peptides could form the basis for future therapeutics, highlighting the need for further exploration of their immunomodulatory potential. - Source: PubMed
Publication date: 2025/10/31
Ciura PiotrGumpelmair SimonSikorska EmiliaRodziewicz-Motowidło SylwiaSteinberger PeterSpodzieja MartaSieradzan Adam K