Mouse Anti-Human CD160
- Known as:
- Mouse Antibody toHuman CD160
- Catalog number:
- 129-10104
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD160
Related genes to: Mouse Anti-Human CD160
- 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: Mouse Anti-Human CD160
Related articles to: Mouse Anti-Human CD160
- Preeclampsia is a multifactorial pregnancy complication characterized by hypertension and immune dysregulation, which can lead to adverse maternal and fetal outcomes. Decidual immune cells are critical for pregnancy homeostasis, yet their functional abnormalities and mechanisms in preeclampsia remain poorly understood. Herein, we sorted decidua immune cells from preeclampsia patients for single-cell RNA sequencing to characterize cellular composition and functional heterogeneity. We delineated the immune cell landscape of the decidua in preeclampsia. A hallmark of decidual immune microenvironment in preeclampsia was the marked augmentation of cytotoxic activity. Both NK and T cells exhibited enhanced cytotoxic activity, characterized by the significant upregulation of cytotoxicity-associated genes. NK cells exhibited a differentiation predisposition toward a unique tissue-resident ITGAECD160 subset with heightened cytotoxic and chemokine gene expression. Cell-cell communication analysis further revealed strengthened interactions between NK cells and macrophages, with macrophage-derived SPP1 signals potentially contributing to the amplification of local cytotoxic responses. Collectively, this study provides a comprehensive single-cell analysis of cytotoxic immune changes at the maternal-fetal interface in preeclampsia, revealing enhanced cytotoxicity that may represent a key pathological mechanism. These insights may inform the development of diagnosis and therapeutic strategies targeting cytotoxic immune dysregulation in PE. - Source: PubMed
Publication date: 2026/04/16
Mu YueliLiu DongHe ZhuoxuWang JulinZhou WenjieChen HongqinZhou ShengpingFeng TingZhou RongLi Hong - Sea turtles are among the many wildlife species adversely affected by Florida red tide, Karenia brevis. This marine dinoflagellate blooms almost annually along Florida's west coast and produces brevetoxins, a suite of potent neurotoxins. Brevetoxins can reach carnivorous loggerhead and Kemp's ridley sea turtles via aerosols and marine food webs, leading to multi-system physiological effects. Sea turtles stranded during red tide can be rescued, transported to rehabilitation facilities, and given palliative care with the goal of return to the wild. However, there are no definitive diagnostic criteria for brevetoxicosis other than stranding in association with red tide. Often sea turtles experience delayed exposure due to the long temporal scale of trophic transfer of toxins. To identify exposure biomarkers and to better understand the mechanism of toxicity of brevetoxins, plasma samples from red-tide exposed and healthy loggerhead and Kemp's ridley sea turtles were analyzed via bottom-up TMT-labeled quantitative liquid chromatography tandem mass spectrometry-based proteomics. Multiple sea turtle plasma protein abundances were significantly altered in red tide exposed turtles, including several immune system proteins like serum amyloid A5 (SAA-5; loggerheads) and CD160 antigen (Kemp's ridley). Pro-inflammatory markers serum amyloid A (SAA) and myeloid-related protein 126 (MRP-126) were measured independently in plasma of loggerhead turtles, with significant increases in these markers with red tide toxin exposure. The two species also differed in their proteomic response to red tide, indicating distinct biomarker candidates. Amid intensifying red tide events and the endangered status of these species, our findings provide a foundation for biomarker-based diagnosis of brevetoxicosis in sea turtles. - Source: PubMed
Publication date: 2026/04/13
Ceballos CelinaRein Kathleen SWalsh Catherine J - Bladder cancer (BC) is a common malignancy with high recurrence and substantial monitoring costs. Limitations of current diagnostic tools: cystoscopy is invasive and expensive, urine cytology lacks sensitivity and existing urine biomarkers cannot replace cystoscopy, underscoring the need for improved non-invasive methods. Immune checkpoints (ICs) regulate immune activity, and newer ICs: T-cell immunoglobulin and mucin domain 3 (TIM-3), galectin-9 (Gal-9), B- and T-lymphocyte attenuator (BTLA), herpesvirus entry mediator (HVEM), cluster of differentiation 160 (CD160), and lymphocyte-activation gene 3 (LAG-3), are involved in cancer immune evasion. This study demonstrated that levels of soluble ICs (sICs) are markedly elevated in patients with early-stage BC. Serum levels of sTIM-3, sGal-9, sBTLA, sHVEM, sCD160, and sLAG-3 were quantified in BC and controls. sTIM-3, sGal-9, and sBTLA were significantly elevated in BC, while their concentrations didn’t vary by tumor stage or grade, supporting diagnostic rather than prognostic utility. Whereas sHVEM, sCD160, and sLAG-3 showed no diagnostic value. Age, sex, and body mass index (BMI) had minimal influence on sIC levels. Receiver operating characteristic (ROC) analyses showed strong performance: sGal-9 was the best classifier (area under the curve (AUC) = 0.98; 91% sensitivity; 100% specificity), followed by sTIM-3 (AUC = 0.91) and sBTLA (AUC = 0.78). sHVEM, sCD160, sLAG-3 performed poorly. A multivariate model incorporating sGal-9, sTIM-3, and sBTLA achieved a cross-validated AUC = 0.982, with sGal-9 remaining independently predictive. Correlation analyses revealed two clusters: sGal-9/sTIM-3/sBTLA and sHVEM/sCD160, that relationships align with known receptor-ligand biology and may reflect shedding during T-cell exhaustion. Overall, sGal-9, supported by sTIM-3 and sBTLA, constitutes promising serum biomarker panel associated with early-stage BC, however, as these markers are not disease-specific and may be affected by inflammatory or other pathological conditions, further validation is required. - Source: PubMed
Publication date: 2026/04/14
Andrzejczak AnnaKrajewski WojciechJaskuła EmiliaChorbińska JoannaTomkiewicz AnnaSarat KrystianMroczek RobertMałkiewicz BartoszSzydełko TomaszKarabon Lidia - 1.6 billion people are currently infected with parasitic worms. Group 2 innate lymphoid cells (ILC2) play a central role in promoting the protective type 2 immunity against these parasites. Here we show that a subpopulation of intestinal ILC2 express the immune checkpoint molecule CD160 in mice infected with the parasitic nematode Strongyloides ratti. CD160 ILC2 represented a distinct ST2IL-17RBKi-67 subset that expanded in vivo during S. ratti infection. By contrast, CD160 ILC2 were ST2IL-17RBKi-67 and represented the dominant producers of type 2 cytokines. Upon in vitro stimulation, sorted CD160 ILC2 progressively lost CD160 expression and acquired cytokine-producing capacity. While CD160-competent RAG KO mice efficiently controlled S. ratti infection with less than 1% of the infective dose remaining by day 10 post-infection, CD160-deficient RAG KO mice failed to expand intestinal ILC2, failed to activate mucosal mast cells and retained high intestinal worm burden for nearly 100 days. Adoptive transfer of CD160-competent ILC2 into S. ratti-infected CD160-deficient RAG KO mice partially restored mast cell activation and reduced intestinal worm burden by 50%. Collectively, these findings identify CD160 expression as a critical checkpoint in the development and expansion of fully functional ILC2 required for effective immunity against intestinal helminth infection. - Source: PubMed
Publication date: 2026/04/12
Heepmann LennartHartmann WiebkeLinnemann LaraDörken SaraViebrock BirteOrinska ZaneJacobs ThomasMcSorley Henry JBreloer Minka - Tumor spatial architecture significantly influences immune responses, but the impact of regional variations on T cell exhaustion and clonality in human papillomavirus (HPV)-related cervical squamous cell carcinoma (CESC) remains poorly understood. Using single-cell RNA sequencing (scRNA-seq, n = 13) and TCR sequencing (scTCR-seq, n = 9), this study profiled T cells from paired tumor core and edge samples of patients with CESC. This was supplemented by bulk RNA-seq data (n = 41), TCGA datasets from three cancer types (CESC, head and neck squamous cell carcinoma, and lung squamous cell carcinoma), and scRNA-seq data from colorectal cancer for broader validation. We found that CD8 T cells, natural killer T (NKT) cells, and γδ T cells in the tumor core exhibited higher inhibitory and cytotoxicity scores, while CD4 T cells showed increased regulatory T (Treg) and cytotoxic features in the tumor core. Bulk RNA-seq data confirmed elevated inhibitory and cytotoxic scores in the tumor core relative to the edge. Additionally, four subsets of exhausted CD8 T cells (CD8 Tex) were identified, including a stress-associated subset characterized by heat shock protein (HSP) family gene expression, which was validated by immunofluorescence and inversely correlated with survival in patients with CESC undergoing radiotherapy. TCR analysis revealed clonal expansion and reduced clonal diversity in the tumor core. Notably, CD8 Teff-CD160 cells displayed substantial clonal sharing across regions and were associated with a favorable prognosis. Overall, our findings highlight distinct T cell states between the tumor core and edge in HPV-related CESC, offering insights into prognostic biomarkers and potential therapeutic targets. - Source: PubMed
Lei TianyuWang FuhaoZhang ShuominZhang LiangWei HongfuLi YixuanHuang QingyuLiu XiangXia LiangbinWang CongLiu ChaoHu Qinyong