Recombinant Human CD69 /CLEC2C Protein
- Known as:
- Recombinant Human CD69 /CLEC2C Protein
- Catalog number:
- cd-756
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human CD69 /CLEC2C Protein
Related genes to: Recombinant Human CD69 /CLEC2C Protein
- Gene:
- CD69 NIH gene
- Name:
- CD69 molecule
- Previous symbol:
- -
- Synonyms:
- CLEC2C
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-06
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human CD69 /CLEC2C Protein
Related articles to: Recombinant Human CD69 /CLEC2C Protein
- Malaria remains a significant public health concern despite a steady decline in symptomatic cases. In Brazil, endemic regions are primarily concentrated in the Amazon region, where most cases are attributed to Plasmodium vivax. Although malaria does not confer long-term sterilizing immunity, clinical immunity is achieved, leading to asymptomatic (ASY) infections. Assessing cellular immunity against P. vivax is challenging due to the lack of well-defined antigens. Hence, we developed a library of 310 P. vivax peptides (MPv310) to evaluate antigen-specific responses of CD4+ T cells and their memory subpopulations. The specific cytokine response, IFN-γ and TNF, and upregulation of activation markers, CD69 and CD154, were assessed in P. vivax-infected individuals, including symptomatic before treatment (SY-I) patients, symptomatic after treatment (SY-T) patients, ASY individuals, and uninfected individuals. CD4+ T cells were stimulated with peptides and analyzed by flow cytometry or ELISpot. MPv310 stimulation led to increased frequencies of CD154+ and CD69+CD154+ cells in symptomatic before treatment and SY-T patients and IFN-γ+TNF+ cells in SY-T patients. Cytokine response was also associated with ASY status, with higher frequencies of IFN-γ+TNF+ among CD4+ T cells and of IFN-γ+ in the effector memory subset. Distinct antigen-specific activation patterns were also observed among symptomatic and ASY individuals when the peptide pool was divided into smaller pools representing specific antigens. This study reveals that MPv310 and different sets of minipools stimulate CD4+ T cells in symptomatic and ASY infections, having potential to be used as a new tool to assess immune mechanisms associated with different clinical presentations of the disease and protection against malaria. - Source: PubMed
Costa Camila MedeirosAlmeida Gregório GuilhermeLindestam Arlehamn Cecília SQueiroz-Glauss Camila PereiraGunderman Victor Hugo GonçalvesPereira Marcela Marísia MayrinkAmaral Laurence Rodrigues DoPereira Dhelio BatistaTada Mauro ShugiroMartins-Filho Olindo AssisGazzinelli Ricardo TostesAntonelli Lis Ribeiro Do Valle - Natural killer (NK) cells are critical for early antiviral immunity, yet their metabolic regulation during acute human viral infection remains incompletely understood. We analyzed NK cell activation and metabolic reprogramming in 47 vaccinated individuals with mild breakthrough SARS-CoV-2 infection and 20 matched healthy control subjects. COVID-19 patients exhibited elevated plasma interferon α and NK cell activation markers (CD69, CD38), alongside increased basal STAT5 phosphorylation, consistent with IL-15-mediated signaling. Functionally, NK cells from infected subjects displayed heightened cytotoxicity. Metabolic profiling at the single-cell level revealed increased cell size, translational activity, amino acid and glucose uptake, and mitochondrial membrane potential, indicating a globally activated metabolic state specific to NK cells. Using newly developed spectral cytometry panels targeting metabolic regulators, we identified CPT1a as the most discriminative marker between patient and control NK cells, with elevated expression in both CD56bright and CD56dim subsets. CPT1a levels correlated with CD38 expression and with uptake of the fluorescent palmitate analog BODIPY-FL C16, reflecting enhanced long-chain fatty acid oxidation. These changes were absent in B and T lymphocytes. Our findings support that during SARS-CoV-2 infection, human NK cells undergo coordinated cytokine-driven activation and metabolic remodeling, integrating glycolysis and lipid oxidation to support amplified effector function. - Source: PubMed
Benezech SarahPicq LouisVillard MarineRousseaux NoémiHamond AmelineAllatif OmranBal AntoninBelot AlexandreTrouillet-Assant SophieMarçais AntoineWalzer Thierry - The traditional dichotomy between antibody-mediated rejection (AMR) and T cell- mediated rejection (TCMR) after kidney transplantation is increasingly challenged. While T cell populations and their clonal expansion have been demonstrated in TCMR, the involvement and clonality of T cells remains unexplored in AMR. - Source: PubMed
Publication date: 2026/04/23
Vaulet ThibautLamarthée BaptisteCallemeyn JasperKoshy PriyankaAnglicheau DanyAntoranz AsierDebyser TimChauveau BertrandGwinner WilfriedKuypers DirkLambrechts DietherMarquet PierreRabant MarionSenev AlexanderVanhoutte ThomasNaesens Maarten - Gut microbiota may affect the development of autoimmune (type 1) diabetes by differential potency of intestinal species to induce endotoxin tolerance (ET). However, where ET impinges on immune mechanisms underlying autoimmune diabetes is yet incompletely understood. We investigated the effects of lipopolysaccharide (LPS) from E. coli and B. vulgatus, two common intestinal species dominating either in low- or high-incidence countries, on activation and chemoattraction of islet-specific T cells in non-obese diabetic (NOD) mice. Intraperitoneal (i.p.) injection of E. coli LPS induced costimulatory ligands CD40, CD80 and CD86 on both conventional and cross-presenting (XCR1+) dendritic cells (DC) and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-reactive islet-specific T cells in the pancreatic lymph node. In comparison to mice not primed with E. coli LPS or primed with B. vulgatus LPS, the second injection of E. coli LPS lowered the frequency of IGRP-reactive T cells and CD80 expression on DC subsets, as well as CD44 and CD69 activation markers and the CXCR3 chemokine receptor on IGRP-reactive T cells. In islets, expression of chemokine CXCL10 accentuated, and insulitis became more severe in mice primed with B. vulgatus LPS. Our results provide mechanistic insight into how ET affects islet autoimmunity and suggest that physiological exposure to E. coli LPS may benefit in moderating autoimmune diabetes. - Source: PubMed
Silojärvi Satu MLeino Linda A APöysti Sakari AHänninen Arno L M - Individuals with inborn errors of immunity often mount suboptimal responses to vaccination, yet the molecular determinants underlying their variable responses to mRNA vaccines remain poorly defined. The present study aimed to identify baseline immune transcriptional signatures predictive of humoral responses to the BNT162b2 (Comirnaty) mRNA vaccine in individuals with inborn errors of immunity. Twenty-one SARS-CoV-2-naïve participants with diverse inborn errors of immunity were stratified as high or low responders to the BNT162b2 vaccine based on anti-SARS-CoV-2 spike IgG titers at day 28 post-vaccination. Although vaccine-induced T cell responses were broadly comparable, low responders had significantly lower frequencies of switched memory B cells ( = .014). Transcriptional profiling revealed 41 differentially expressed genes between groups at baseline. Activated memory B cells and peripheral T follicular helper cells from high responders exhibited greater induction of activation and memory-related genes, including NFKB1, CD69, TIGIT, CD40L, and BATF, indicating greater intrinsic readiness to support coordinated antibody production. These findings demonstrate that distinct pre-vaccination gene expression patterns within specific immune subsets are associated with differential humoral responses to mRNA vaccination in individuals with inborn errors of immunity. More broadly, the study highlights that baseline molecular immune features substantially influence vaccine efficacy and suggests that pre-vaccination transcriptional profiling may enable more personalized vaccination strategies for individuals with impaired immunity. - Source: PubMed
Publication date: 2026/04/24
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