TNFSF18 Antibody (Center) Blocking Peptide
- Known as:
- TNFSF18 Antibody (Center) Blocking Peptide
- Catalog number:
- BP16250c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- TNFSF18 Antibody (Center) Blocking Peptide
Related genes to: TNFSF18 Antibody (Center) Blocking Peptide
- Gene:
- TNFSF18 NIH gene
- Name:
- TNF superfamily member 18
- Previous symbol:
- -
- Synonyms:
- AITRL, TL6, hGITRL
- Chromosome:
- 1q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-15
- Date modifiied:
- 2017-03-02
Related products to: TNFSF18 Antibody (Center) Blocking Peptide
Related articles to: TNFSF18 Antibody (Center) Blocking Peptide
- Classic Hodgkin lymphoma (CHL) is a highly curable disease. However, a subset of patients develops relapsed/refractory disease, underscoring the need for predictors of treatment response. Although immune-checkpoint inhibitors have improved outcomes, many patients still experience suboptimal responses. A deeper understanding of the CHL transcriptomic landscape may improve patient stratification and guide treatment approaches. Targeted mRNA-NGS was performed on formalin-fixed paraffine-embedded CHL-tissue using the HTG EdgeSeq Precision Immune-Oncology Panel (1,392 genes) in treatment-naive and post-chemotherapy relapsed treated with nivolumab-based protocols. Differential gene expression and pathway enrichment analyses were conducted to characterize tumor-intrinsic, and microenvironmental features associated with disease biology and treatment response. Across all CHL samples (n = 25) we observed overexpression of immune-checkpoint and immunoregulatory genes (CD274, CTLA-4, IL6, IL13), and markers of macrophage-rich/matrix-remodeling microenvironment (CD163, MMP2, TIMP1), alongside loss of B-cell identity and tumor suppression programs. Pathways analysis revealed activation of IL6/JAK/STAT3, TNF-α/NF-κB, KRAS-UP, and Inflammatory response, with reduced proliferative and metabolic activity. Immunotherapy non-responders, both in the overall (n = 5; 20%), and the treatment-naïve CHL (n = 2; 12%) displayed a proliferative, cytokine-activated, and immunologically cold phenotype. This includes shared overexpression of FADD, NFKB1, and TGFB1 and downregulation of SMAD7, together with activation of E2F, G2M, MYC, and PI3K/AKT/mTOR pathways and negative enrichment of TNF-α/NF-κB, IL6/JAK/STAT3, and Inflammatory response. Post-chemotherapy relapsed (n = 8) exhibited adaptative immunoregulatory and stress response signatures (IL15, TNFSF18, MAPK8, FUT4), along with reduced immune activation and loss of tumor-suppressor signaling. This study highlights the biological complexity and transcriptional diversity underlying CHL and its tumor microenvironment. Immunotherapy non-responders exhibited an "oncogene-driven" transcriptional profile independent of previous treatment status, whereas responders showed an "inflammatory immune-scape" phenotype, offering insight into mechanisms of resistance. Despite the limited sample size, these findings provide a foundation for larger precision-focused studies aimed at improving outcomes in CHL. - Source: PubMed
Publication date: 2026/08/05
Hamana LeticiaMarques-Piubelli Mario LWei LuKhan KhajaKakarala LakshmiShen LiWistuba Ignacio ILee Hun JuSolis Luisa MVega Francisco - Regulatory T cells play a pivotal role in shaping immune interactions, limiting antitumor immunity, and impairing the activity of engineered effector cells. Overcoming regulatory T (Treg) cell-mediated immunosuppression is critical to unlock the full therapeutic potential of chimeric antigen receptor (CAR)-cell therapies. Here, we develop "armored" anti-CD19 CAR-NK cells coexpressing GITR ligand (GITRL) (CAR19-GITRL-NK) to both target malignant B cells and locally counteract Treg-mediated suppression. GITR is highly expressed on Tregs, and engagement by its ligand GITRL can modulate their function, providing a rational strategy to reprogram the tumor microenvironment. - Source: PubMed
Publication date: 2026/07/07
Schmidt DayaneEbrahimabadi SimaTirapelle Mariane CariatiGarcia Ferreira Camilly MeloDos Santos Matheus HenriqueBiggi Alison Felipeda Silva Januário Mara ElisamaCalado Rodrigo TocantinsPicanço-Castro Virginia - Anaplastic thyroid carcinoma (ATC) may arise from the progression of differentiated thyroid cancers, but the mechanisms are not well understood. Establishing appropriate animal models and conducting ultrasound imaging monitoring can facilitate the study of this dedifferentiation process. - Source: PubMed
Publication date: 2026/06/28
Jin AnqiWang ShiyuWang JianYu PengchengWang YulongShi JunZhou Shichong - Prostate cancer (PCa) is prototypically immunologically "cold", characterized by low tumor mutational burden, sparse CD8 T-cell infiltration, and resistance to immune checkpoint blockade. The tumor cell-intrinsic programs driving immune evasion in this context remain incompletely defined. - Source: PubMed
Publication date: 2026/03/18
Liu WeihaoLi GuopingLei YanLiu HuixiuWang BinhuiDeng WeimingHong YudeLong Xiangyang - The hostile tumor microenvironment (TME) remains a major challenge for cancer immunotherapy. In this study, we performed TME-targeted in vivo CRISPR activation (CRISPRa) screen to identify factors that promote antitumor immunity, culminating in rationally designed immune gene therapy combinations. Multiplexed activation of genes encoding antigen presentation, T-cell proliferation, costimulation, and migration (APCM) leads to enhanced antitumor responses. An APCM-focused CRISPRa screen in metastatic tumors identified Cd80, Tnfsf14, Cxcl10, Tnfsf18, Tnfsf9, and Ifng as top immunostimulatory candidates. Further optimization pinpointed Tnfsf9 (4-1BBL) + Ifng + Il12b (4II) as a potent therapeutic combination. Adeno-associated virus (AAV) 4II enhanced antigen presentation, T-cell activation, proliferation, cytotoxicity, and tumor infiltration. Preconditioning the TME with AAV-4II synergized with chimeric antigen receptor (CAR) and T-cell receptor (TCR) T-cell therapies to suppress primary and metastatic solid tumors in vivo. These findings establish TME-targeted CRISPRa screening as a rapid route to develop immune gene therapy combinations against solid tumors. - Source: PubMed
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