Anti_Human, mab CD94 Source Mouse
- Known as:
- Anti_Human, mab CD94 Source Mouse
- Catalog number:
- 101-M319
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CD94 Source Mouse
Related genes to: Anti_Human, mab CD94 Source Mouse
- Gene:
- KLRD1 NIH gene
- Name:
- killer cell lectin like receptor D1
- Previous symbol:
- CD94
- Synonyms:
- -
- Chromosome:
- 12p13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-16
- Date modifiied:
- 2016-01-14
Related products to: Anti_Human, mab CD94 Source Mouse
Related articles to: Anti_Human, mab CD94 Source Mouse
- Meningococcal Serogroup A conjugate vaccine, as compared to the polysaccharide vaccine, has been clinically proven to induce superior protective immune responses against serogroup A infection in infants and young children. Studies examining the immune pathways/biomarkers responsible for the superiority of conjugate over plain polysaccharide vaccines are greatly required. This study reports the comparative whole blood transcriptomic profiles of the late-stage immune responses induced by meningococcal polysaccharide and conjugate vaccine in a murine model. Unique peripheral gene transcripts were induced by the Men A PS-tetanus toxoid (Men A PS-TT) vaccine compared to the Men A PS-alum (Men A PS-ALPO4) vaccine. Conjugate vaccine reported significant expression for Actb, Cd1d1, Klra8, Klrd1, Tnf, and H2-Q10 genes. Whereas plain polysaccharide vaccine reported key changes for Itga2b, H2-Ab-1, Cd8b1, and Icam2 genes. Annotation studies reported markers related to cytokine and chemokine activation, T and B cell activation, NKT-cell mediated cytotoxicity, antigen processing and presentation, and complement activation were differentially expressed in the conjugate vaccine as compared to the polysaccharide vaccine. The study reports late-stage immune markers that could be potential biomarkers for a better understanding of pathways responsible for immunity to T cell-dependent and independent antigens. - Source: PubMed
Publication date: 2026/04/04
Patel KrunalGautam ManishGairola Sunil - Antibody-mediated rejection (ABMR) in heart transplants is often negative for donor-specific antibody (DSA). We explored potential molecular differences between DSA-negative and DSA-positive molecular ABMR in 212 heart endomyocardial biopsies from the prospective Trifecta-Heart study (NCT04707872). - Source: PubMed
Publication date: 2026/03/13
Madill-Thomsen Katelynn SHidalgo Luis GMackova MartinaDemko ZachPrewett AdamCampbell PatrickFelius JoostGong TimothyHall ShelleyKim Daniel HKuczaj AgnieszkaLowe DaveMaliakkal NevilleMelenovsky VojtěchOlympios MichaelPatel SnehalPrzybylowski PiotrSayer GabrielTseliou EleniUriel NirStehlik JosefHalloran Philip F - The molecular mechanisms underlying adaptation to physical exertion and racing stress in horses remain incompletely understood. Peripheral blood transcriptomics offers a minimally invasive method to monitor systemic responses to exercise and identify biomarkers of adaptation or overload. - Source: PubMed
Publication date: 2026/03/07
Dąbrowska IzabelaGrzędzicka-Agko JowitaKiełbik PaulaTrela MichałWitkowska-Piłaszewicz Olga - Natural killer (NK) cells expressing inhibitory receptors that recognize self human leukocyte antigen (HLA) class I molecules gain enhanced functionality-a process influenced by genetic polymorphism that dictates the strength of interactions between inhibitory receptors and their HLA ligands. Inhibitory CD94/NKG2A binds HLA-E loaded with epitopes derived from polymorphic HLA class I signal peptides (SPs). We generated a metric, called SP score, that quantifies the overall strength of CD94/NKG2A-HLA-E interactions based on a person's SP genotype. SP scores correlated positively with NKG2ACD56 NK cell response to HLA class I-negative cells, indicating that CD94/NKG2A-HLA-E interaction strength promotes NK cell education. Concordantly, higher SP scores associated with lower risk of nasopharyngeal carcinoma and ulcerative colitis. Thus, the SP score may serve as a genetic tool to guide clinical NK cell intervention strategies, including therapeutic NKG2A blockade. - Source: PubMed
Publication date: 2026/03/04
Lin ZhansongBashirova Arman ACallahan CianNelson George WRobinson EmmaViard MathiasTang MinzhongHildesheim AllanFranke AndreRioux John DGarcia-Beltran WilfredoCarrington Mary - : BK virus (BKPyV) is a common latent pathogen in humans, but it becomes particularly insidious in kidney transplant recipients, where reactivation may contribute to allograft loss. The immune mechanisms controlling BKPyV latency in immunocompromised hosts remain incompletely understood. We assume the urinary immune proteome reflects local immune response in the kidney and the urinary tract. Thus, this study aimed to determine whether the presence of BKPyV alters the urinary immune-related proteomic profile of kidney transplant recipients and shifts it away to that observed in healthy individuals. : 137 urine samples were collected from kidney recipients, both BKPyV-positive and BKPyV-negative, patients with stage 5 chronic kidney disease, and healthy controls. Targeted proteomic analysis was performed using the proximity extension assay, followed by heatmapping, principal component analysis, random forest, and linear regression modeling. : The urinary proteome of BKPyV-positive recipients remained more distinct from healthy controls than that of BKPyV-negative ones. Among the 33 proteins detected across all samples, 17 showed significant intergroup differences, with KLRD1 (CD94) uniquely upregulated in all transplant recipients, but downregulated in BKPyV-positive samples. : We conclude that the presence of BKPyV in the urinary tract of kidney recipients notably interplays with the local immune response even in the absence of clinical disease. - Source: PubMed
Publication date: 2026/01/23
Michnowska AgataWojciuk BartoszReus PaulinaFilipowska AgataMnichowska-Polanowska MagdalenaGrygorcewicz BartłomiejCiechanowski KazimierzKędzierska-Kapuza Karolina