Ask about this productRelated genes to: CD160 antibody
- Gene:
- CD160 NIH gene
- Name:
- CD160 molecule
- Previous symbol:
- -
- Synonyms:
- BY55, NK1, NK28
- Chromosome:
- 1q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-02
- Date modifiied:
- 2016-10-05
Related products to: CD160 antibody
Related articles to: CD160 antibody
- Regulatory T cells (Treg) play a central role in maintaining immune homeostasis, and the implementation of in vitro induced Treg cells (iTreg) to control immune function has significant potential in clinical medicine. The clinical application of iTreg has been limited by their poor stability. To better define the molecular characteristics of human iTreg, we performed a data-independent acquisition proteomics, detecting over 8000 proteins and providing a quantitative comparison of their relative levels in iTreg and activated Th0 cells. Consistent with the known molecular characteristics of Treg, several Treg signature proteins, including FOXP3, IKZF4, IL2RA, CTLA4, PD-1, IKZF3, LAG3, RUNX1 and HIC1, were identified and validated using Tier 2 targeted SRM and/or qRT-PCR. Notably, Leupaxin (LPXN) level was upregulated during Treg cell differentiation. Functional studies demonstrated that LPXN-deficient cells showed impaired expression of Treg protein markers FOXP3, IKZF4 and IKZF3 and impaired suppression of effector T cells. In addition, we identified a distinct CD160 iTreg subpopulation characterized by a distinct proteomic signature as compared to CD160 iTreg. Together, these findings provide a high-resolution proteomic landscape of human iTreg and identified a novel role of LPXN in the development and suppressive activity of iTreg. - Source: PubMed
Publication date: 2026/08/20
Batkulwar KedarAndrabi Syed Bilal AhmadKattelus RoosaBuchacher TanjaArnkil IlonaStarskaia InnaRasool OmidMoulder RobertLahesmaa Riitta - Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis (EBV-HLH) is a life-threatening hyperinflammatory syndrome paradoxically characterized by excessive cytokine production and immune activation despite failure to clear Epstein-Barr virus (EBV). The cellular mechanisms underlying immune dysregulation in EBV-HLH remain incompletely understood. - Source: PubMed
Publication date: 2026/08/05
Luo XiaodanChen AoLiu JianboShi BoyunTang JianliHuang JiayuYuan DanyunLiang ZhimingTan HuoZheng Runhui - Immune checkpoint inhibitors (ICIs) have improved cancer outcomes; however, many patients fail to respond, highlighting the need for novel targets. HVEM (Herpes Virus Entry Mediator) is an immune regulator with both inhibitory and stimulatory functions, making it a promising therapeutic candidate. We have developed Anti-4CB1, a fully human monoclonal antibody (mAb) that selectively blocks HVEM interactions with BTLA and CD160. Its activity was evaluated in-vitro using human tumor-infiltrating lymphocytes (TILs), peripheral blood mononuclear cells (PBMCs), and M1 macrophages, as well as in ex-vivo patient-derived tumor samples and in-vivo transgenic and humanized mouse models. HVEM expression was also assessed in serum and tumor tissues. Anti-4CB1 enhanced T-cell activation and cytotoxicity, evidenced by increased tumor cell killing, upregulation of activation markers (41BB, CD107a), and elevated IFNγ and TNFα secretion. It also promoted macrophage-mediated phagocytosis. In ex-vivo analyses of 49 patient-derived tumor samples, Anti-4CB1 increased cytotoxicity in 28.5% of cases, including samples unresponsive to anti-PD1. In-vivo, Anti-4CB1 demonstrated significant anti-tumor activity as monotherapy and showed enhanced efficacy in combination with anti-PD1. Additionally, higher tumor HVEM expression correlated with improved response to checkpoint blockade, while elevated soluble HVEM levels were associated with reduced responsiveness to Anti-HVEM. Anti-4CB1 enhances both adaptive and innate anti-tumor immunity and shows activity in anti-PD1 resistant settings. These findings support its potential as a novel therapeutic agent and suggest HVEM as a predictive biomarker for immunotherapy response. - Source: PubMed
Publication date: 2026/08/19
Galore-Haskel GilliMerhavi-Shoham EfratShapiro MikaBareli RoniDror NaamaSeliktar-Ofir SivanShamalov KaterinaLandstein DoritLevy-Barda AdvaHout-Siloni GoniSchachter JacobSadot EranEitan RamBarshack IrisGolan ShayFeferman YaelYeoshoua EffiEyadat SaebGreenberg EyalMarkel Gal - CD244, expressed in the tumor microenvironment (TME), is associated with impaired function of natural killer (NK) and T cells; however, its role in diffuse large B-cell lymphoma (DLBCL) remains poorly understood. This study aimed to elucidate the immunological significance and regulatory mechanisms of CD244 in DLBCL. - Source: PubMed
Publication date: 2026/07/07
Yang YimingZeng BiyangYang HuiminLiu XinLi PeilinMai ChaoJian ShunhaiZhu Qiqi - Aberrant activation of SHH signaling contributes to the progression of multiple malignancies, with KIF7 functioning as a critical mediator that regulates signal transduction from SMO to GLI transcription factors. However, the specific role of KIF7 in ccRCC has not been fully elucidated. In this study, we investigated the expression pattern, prognostic significance, functional role, and potential mechanisms of KIF7 in ccRCC. Analysis of TCGA-KIRC data demonstrated that KIF7 expression was significantly elevated in tumor tissues compared with adjacent normal tissues. High KIF7 expression was strongly associated with advanced pathological stage and poor overall survival. IHC performed on commercial tissue microarrays further confirmed increased KIF7 protein levels in ccRCC samples. Functional experiments in the 786-O cell line revealed that KIF7 overexpression markedly enhanced cell proliferation. Mechanistically, KIF7 overexpression activated the Wnt/β-catenin signaling pathway and upregulated downstream cell cycle regulators, including c-Myc and c-Jun. KIF7 expression was positively correlated with infiltration of CD4 + T cells, macrophages, and neutrophils. Moreover, it showed significant positive associations with immune checkpoint molecules PDCD1 and CD160. GSCA/GDSC-based drug sensitivity prediction suggested that high KIF7 expression was associated with increased predicted sensitivity to docetaxel and bleomycin, whereas no significant association was observed for I-BET-762. In conclusion, KIF7 plays a tumor-promoting role in ccRCC by enhancing proliferation, activating Wnt/β-catenin signaling. Additionally, it was associated with shaping the immune microenvironment. These findings highlight KIF7 as a potential prognostic biomarker and therapeutic target in ccRCC. - Source: PubMed
Publication date: 2026/06/28
Wang YaoWang Xiao-MingHuo DaWang Shi-BoLiu Qian-YiPang JingShen TaoCui DiZhao Wen-JuanLuo Qing-FengLi NanChen Ai-QunCui Ju