Anti-Mouse CD314 (NKG2D) PE 100 ug
- Known as:
- Antibody toMouse CD314 (NKG2D) PE 100 ug
- Catalog number:
- 12-5873-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD314 (NKG2D) 100
Related genes to: Anti-Mouse CD314 (NKG2D) PE 100 ug
- Gene:
- KLRK1 NIH gene
- Name:
- killer cell lectin like receptor K1
- Previous symbol:
- D12S2489E
- Synonyms:
- NKG2D, KLR, NKG2-D, CD314
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-12
- Date modifiied:
- 2016-10-05
Related products to: Anti-Mouse CD314 (NKG2D) PE 100 ug
Related articles to: Anti-Mouse CD314 (NKG2D) PE 100 ug
- The use of natural killer (NK) cells for the treatment of solid tumors such as cholangiocarcinoma has been hindered by challenges related to cell production, persistence and trafficking, as well as by reduced efficacy within an immunosuppressive tumor microenvironment. Antitumor immunity can be reduced by the interaction of NK cell expressed programmed cell death protein 1 (PD1) with ligands on tumor and other cells within the tumor microenvironment. The antitumor effect of NK cells is enhanced in cells engineered to express a truncated PD1 without an intracellular domain. The cytolytic potential and therapeutic efficacy of extracellular vesicles (EVs) derived from human NK cells expressing truncated PD1 was evaluated as a cell-free therapeutic to overcome some limitations faced by cell therapies. We demonstrate the feasibility of efficient expansion, production and isolation of therapeutic vesicles from human NK cell lines and from engineered NK92 cells expressing truncated PD1. The cytotoxic efficacy of these therapeutic vesicles was validated in both monolayer tumor cell cultures and in multicellular tumor spheroids. Concomitant administration of gemcitabine upregulated NKG2D ligands on tumor cells and increased susceptibility to NK cell and to NK cell derived EV mediated killing. These findings position engineered NK cell derived-EVs as a scalable and promising cell-free immunotherapeutic for cholangiocarcinoma. - Source: PubMed
Gondaliya PiyushZinn Dylan ASayyed Adil AliDriscoll JuliaYan Irene KMensali NadiaWälchli SébastienPatel Tushar - One of the key hallmarks of aging is the age-related decline in immune system function, accompanied by a chronic low-grade inflammation, or "inflammaging". Simultaneously, a reduced capacity of immune cells to recognize and eliminate pathogens, along with immune exhaustion, is also defined as a sign of aging. Cynomolgus macaques () belong to a group of non-human primates evolutionarily close to humans and are often used for preclinical research. - Source: PubMed
Publication date: 2026/08/13
Petrova Viktoria MBulgin Dmitry VRadomskaya Elena YuShevelov Vsevolod AZhukova Darya SChzhu Olga PManakhov Andrey DPopov Alexander VRybtsov Stanislav A - Stem cell-derived β (SC-β) cells are a promising therapy for type 1 diabetes (T1D), but their long-term efficacy is limited by immune-mediated graft rejection. Platelet-derived exosome product (PEP) has emerged as a novel immunomodulatory agent, although its effect on SC-β cell xenograft rejection remains unclear. Here, we evaluated PEP in stimulated human peripheral blood mononuclear cells (PBMCs) and in an immunocompetent mouse model of SC-β cell transplantation under the kidney capsule. Immune-related gene expression was assessed by quantitative PCR, immune cell infiltration by immunofluorescence, and graft function by circulating human insulin. In vitro, PEP reduced NK-cell-associated gene expression, including NK1.1, EOMES, and KLRK1, and increased IL-10 expression. In vivo, untreated SC-β cell xenografts showed progressive immune infiltration and loss of detectable human insulin by day 14, whereas PEP-treated grafts retained detectable insulin through day 14 across co-transplantation, pretreatment, and systemic administration strategies. PEP co-transplantation delayed, but did not prevent, xenograft rejection, with graft loss observed by day 21. This delay was associated with reduced NK1.1+ cell infiltration and lower expression of selected inflammatory and rejection-associated markers, including NK1.1, Nos2, and Nlrp3. These findings suggest that PEP modulates graft-associated immune responses and may serve as an adjunct immunomodulatory strategy for stem cell-based therapies for type 1 diabetes. Further studies are needed to evaluate sustained graft durability, safety, and translational efficacy. - Source: PubMed
Publication date: 2026/07/29
Khashim ZenithShrestha SwikritiHassoun ShaimaaLaw Ethan WSchornack Anna Marie RLacap JessicaBeetler Danielle JWeigel Gabriel JJennings Lauren TBecher LauraParadise ChrisBehfar AttaFairweather DeLisaPeterson Quinn P - The aim of this study was to detect genomic regions and genes associated with gastrointestinal nematodes (GIN) resistance in Pelibuey sheep, based in deworming necessity (NOD) estimated by fecal egg count (FEC). During a ten-months period, deworming criterion was based on GIN eggs per gram (EPG), then animals exceeding 1000 EPG were dewormed, and individuals were classified as cases (dewormed at least once) or controls (non-deworming at all). Animals were genotyped with the GGP Ovine50k genome profiler microarray. Quality control of dataset and case-control GWAS were carried to identify associated candidate genes and quantitative trait loci (QTL). Two genome-wide strongly associated SNPs were detected on chromosomes 2 and 3, located near FEC associated QTLs and immune-related genes: GALNT6, KLRK1, KLRD1, CLEC1B, FGF13, TMEM52B, OLR1, and CLEC7A. The identified genes are involved in key defense mechanisms such as mucus synthesis, immune signaling, and natural-killer cell activation, supporting their relevance as candidate genes for GIN-resistance selection in Pelibuey hair-sheep. - Source: PubMed
Publication date: 2026/07/04
Esparza-Acebo Leilany MargaritaOjeda-Robertos Nadia FlorenciaDe La Rosa-Reyna Xochitl FabiolaParra-Bracamonte Gaspar Manuel - Immune-resistant colorectal cancer (irCRC), represented by microsatellite stable/proficient mismatch repair (MSS/pMMR) tumors, responds poorly to immune checkpoint blockade (ICB). Here, we developed an ultrasound-targeted nanodroplet destruction (UTND) strategy combined with surface anti-PD-L1-decorated nanodroplets (PPP@P@map) to enhance ICB responsiveness in MSS colorectal cancer. In CT26 and CMT93 murine subcutaneous MSS colorectal cancer models, PPP@P@map combined with UTND markedly suppressed tumor growth compared with control treatments. Single-cell RNA sequencing identified CAF_Pi16 as a candidate therapy-associated cancer-associated fibroblast subset that showed a treatment-related increase after PPP@P@map + UTND, which was further supported by flow cytometry and multiplex immunofluorescence validation. Mechanistically, UTND induced oxidative stress in tumor cells and promoted the generation of advanced glycation end products (AGEs), which activated the AGE-RAGE/PKCα/NF-κB pathway in CAF_Pi16 and increased CCL7 secretion. CAF_Pi16-derived CCL7 provided a CCR2-dependent functional cue to CD8 T cells. In purified CD8 T cells, CCL7 activated NF-κB-related signalling, enhanced activation and cytotoxic effector features, and promoted NKG2D expression; these effects were attenuated by CCR2 blockade or NF-κB inhibition. Functionally, CCL7 enhanced CD8 T cell-mediated tumor-cell killing, whereas NKG2D blockade reduced this effect and weakened the antitumor efficacy of PPP@P@map + UTND in vivo. Together, these findings reveal a UTND-induced tumor cell-CAF_Pi16-CCL7-CD8+ T-cell signalling axis that enhances NKG2D-associated antitumor immunity and provides a mechanistic basis for further investigation of UTND-based strategies to improve ICB responsiveness in MSS/pMMR colorectal cancer. - Source: PubMed
Publication date: 2026/07/29
Tuo BaojingLi NaLiu SenboGao ShuochenLiu HangPei LipingGao XueyanLi KaiboXu YanxinSun ZhenqiangZhang YanLiu LinWang Chengzeng