TNFRSF1B _ TNFR2 _ CD120b Protein
- Known as:
- TNFRSF1B _ TNFR2 _ CD120b Protein
- Catalog number:
- 10417-H03H
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TNFRSF1B _ TNFR2 CD120b Protein
Related genes to: TNFRSF1B _ TNFR2 _ CD120b Protein
- 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
- Gene:
- TNFRSF1B NIH gene
- Name:
- TNF receptor superfamily member 1B
- Previous symbol:
- TNFR2
- Synonyms:
- TNFBR, TNFR80, TNF-R75, TNF-R-II, p75, CD120b
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2016-06-28
Related products to: TNFRSF1B _ TNFR2 _ CD120b Protein
Related articles to: TNFRSF1B _ TNFR2 _ CD120b Protein
- 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 - Common cancer treatments include radiation therapy, chemotherapy including molecular targeted drugs and anticancer drugs, and surgical treatment. Recent studies have focused on investigating the mechanisms by which immune cells attack cancer cells and produce immune tolerance-suppressing cytokines, as well as on their potential application in cancer immunotherapy. We conducted expression profiling of (), (), (), and () using data of 158 glioblastoma multiforme (GBM) patients with clinical information available at The Cancer Genome Atlas. Principal component analysis of the expression profiling data was used to derive an equation for evaluating the status of Th1 and Th2 cells. GBM specimens were divided based on the median of the Th scores. The results revealed that Th1Th2 and Th1Th2 statuses indicated better prognosis than Th1Th2, and were evaluated based on the downregulation of PD-L1, PD-L2, and PD-1. Furthermore, Th2 divided based on the threshold, as well as CD274 and PDCD1, were associated with good prognosis. In the Th2 subgroup, 14 genes were identified as potential prognostic markers. Of these, SLC11A1, TNFRSF1B, and LTBR also indicated good prognosis. These results suggest that low Th2 balance and low activity of the PD-L1/PD-1 axis predict good prognosis in GBM. The set of genes identified in the present study could reliably predict survival in GBM patients and serve as useful molecular markers. Furthermore, this set of genes could prove to be novel targets for cancer immunotherapy. - Source: PubMed
Publication date: 2018/04/10
Takashima YasuoKawaguchi AtsushiKanayama TomohikoHayano AzusaYamanaka Ryuya - Prenatal maternal stress (PNMS) is an important programming factor of postnatal immunity. We tested here the hypothesis that DNA methylation of genes in the NF-κB signaling pathway in T cells mediates the effect of objective PNMS on Th1 and Th2 cytokine production in blood from 13½ year olds who were exposed in utero to the 1998 Quebec ice storm. - Source: PubMed
Publication date: 2016/05/12
Cao-Lei LeiVeru FranzElgbeili GuillaumeSzyf MosheLaplante David PKing Suzanne