Anti_Mouse, mab TNFRSF3 Source Rat
- Known as:
- Anti_Mouse, mab TNFRSF3 Source Rat
- Catalog number:
- 103-M485
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab TNFRSF3 Source Rat
Related genes to: Anti_Mouse, mab TNFRSF3 Source Rat
- Gene:
- LTBR NIH gene
- Name:
- lymphotoxin beta receptor
- Previous symbol:
- D12S370
- Synonyms:
- TNFCR, TNFR-RP, TNFR2-RP, TNF-R-III, TNFRSF3
- Chromosome:
- 12p13
- Locus Type:
- gene with protein product
- Date approved:
- 1996-03-12
- Date modifiied:
- 2015-11-17
Related products to: Anti_Mouse, mab TNFRSF3 Source Rat
Related articles to: Anti_Mouse, mab TNFRSF3 Source Rat
- Allergic contact dermatitis (ACD) is a chronic inflammatory skin disorder the development of which is driven by allergen sensitization in peripheral lymphoid organs and local cutaneous inflammation. Lymphotoxin (LT) and its receptor LTβR are critical for lymphoid organogenesis and immune regulation in barrier tissues, but their role in ACD pathogenesis remains incompletely defined. This study aimed to delineate differential contribution of the LTβR-dependent signaling in oxazolone-induced dermatitis. We examined Lta knockout (Lta KO) mice, which lack both soluble LTα3 and membrane-bound isoforms LTα1β2/LTα2β1, and the Ltbr knockout (Ltbr KO) mice, both of which lack lymph nodes. ACD was induced by repeated oxazolone application to ear skin, with assessment of clinical severity, inflammation-associated gene expression, serum IgE levels, and immune cell composition in blood and spleen. Contrary to previous reports, the Lta KO mice developed dermatitis comparable to the wild-type (WT) mice, with elevated IgE production. In contrast, the Ltbr KO mice were substantially protected from the disease, exhibiting attenuated clinical inflammation, reduced ear swelling, and decreased expression in the lesional skin at the background of a lower proportion of circulating CD4 T cells. These findings indicate that LTβR-dependent signaling is pathogenic in allergic skin inflammation, while LTα-mediated pathways are dispensable, suggesting a potential role for the other LTβR ligand, LIGHT, in ACD pathogenesis. Notably, ACD developed even in the absence of lymph nodes, highlighting the importance of local, skin-resident LTβR-dependent mechanisms in the disease development. - Source: PubMed
Gorshkova Ekaterina ADrutskaya Marina SNedospasov Sergei AGubernatorova Ekaterina O - Immune checkpoint inhibitors (CPIs) have revolutionized cancer therapy, yet many patients derive limited benefit due to poor immune infiltration within the tumor microenvironment (TME). The presence of tertiary lymphoid structures (TLS) and high endothelial venules (HEVs) correlates with improved immunotherapy responses. This study evaluated whether selective activation of lymphotoxin-beta receptor (LTβR) signalling, targeted to fibroblast activation protein (FAP)-expressing tumor stroma, could remodel the TME to enhance immune cell infiltration and potentiate immunotherapy. - Source: PubMed
Publication date: 2026/04/21
Bianchi RobertaKunz LeoHosse Ralf JBrydon MichelleAmorim AnaSchwalie Petra CSpeziale DarioVarol AhmetAppelt BirteDrozdowicz Elzbietale Clech MarineValdeolivas AlbertoKumpesa NadineHahn KerstinRichardson MarionGiroud NicolasPesti BenedekGassner ChristianWimmer ReinerHenniger LouisaVillenave RemiBoetsch ChristopheHopfer UlrikeBessa JulianaTrumpfheller ChristineMajety MeherUmaña Pablo - 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 - Pancreatic ductal adenocarcinoma (PDAC) is strongly resistant to immunotherapy. However, recent evidence shows that some PDAC tumors contain tertiary lymphoid structures (TLSs) associated with improved survival. Why TLS forms in some tumors but not others remains elusive. Using a lymphotoxin beta receptor (LTBR) agonist, we observe the induction of TLS-aggregates in some murine PDAC tumor models but not others. The phenotypes of cancer-associated fibroblasts (CAFs) in TLS-resistant models are myofibroblastic (myCAF), whereas TLS-permissive models are enriched with reticular-CAF (rCAF) subsets. Differentiation into myCAF blocks the LTBR-mediated upregulation of chemokines and lymphocyte migration toward fibroblasts. Inhibiting the transforming growth factor β (TGFβ) receptor, combined with LTBR agonism, promotes TLS formation and T cell-dependent tumor control. In patient tumors, rCAF are proximal to TLS, while myCAF are distally located. These data indicate that myCAF represses rCAF programming critical for TLS formation but can be therapeutically remodeled to promote immune control of PDAC tumors. - Source: PubMed
Publication date: 2026/03/26
Kirschstein ElijahHarder OliviaKrull JordanSikorski MadisonKhanal ShrijanMack MorganWare Carl FEvans ElizabethGough Michael JMa QinChen WeiYoung Kristina HGunderson Andrew J - RASSF1A is a well-established tumor suppressor implicated in various human malignancies; however, its specific role in the metastasis of gastric cancer (GC) remains poorly understood. In this study, we observed that RASSF1A expression is frequently silenced in GC tissues compared to adjacent normal tissues, with its loss significantly correlating with metastatic progression. Immunohistochemical analysis further revealed a negative correlation between RASSF1A levels and the infiltration of neutrophils, as well as the formation of neutrophil extracellular traps (NETs). Mechanistically, knockdown of RASSF1A triggers the JNK-JUN signaling pathway, which subsequently accelerates ribosome biogenesis. This metabolic shift enhances the translation of pro-inflammatory chemokines, thereby promoting neutrophil recruitment and NETs formation. Furthermore, our findings demonstrate that RASSF1A interacts with LTBR, effectively inhibiting the LIGHT-induced recruitment of TRAF2 and suppressing downstream JNK-JUN activation. Collectively, our results suggest that RASSF1A functions as a critical inhibitor of GC metastasis by modulating the chemokine-neutrophil axis, offering novel insights into its role as a therapeutic target in GC. - Source: PubMed
Publication date: 2026/03/14
Chen YuDai LingchenChen GuohaoDeng ShukangLiu RuiqingXue WanjiangHu YilinYi Jianfeng