CD69 protein
- Known as:
- CD69 protein
- Catalog number:
- 80R-4395
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- CD69 protein
Ask about this productRelated genes to: CD69 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: CD69 protein
Related articles to: CD69 protein
- The cellular immune response underlying post-injury multiple organ dysfunction syndrome (MODS) remains incompletely described. We hypothesized that early perturbations in innate lymphocyte behavior are critical to the development of MODS in trauma patients. To address this, we examined lymphocyte subsets in a prospective cohort of major trauma patients recruited at a single major trauma hospital. Circulating lymphocytes were profiled with flow cytometry in serial samples drawn within the hyperacute (≤2 h) and acute (24 h, 72 h) post-injury periods. Plasma levels of specific mediators derived from innate lymphocytes were also measured in a larger cohort. We observed a marked hyperacute increase in circulating NK (particularly the CD56 subset) and Vδ1 cells that were associated with MODS or early mortality. Absolute counts of NK activation markers CD69 and NKG2D were also higher in patients with adverse outcomes, although the proportion of NK cells expressing NKG2D was reduced. Exploratory cluster analyses of NK activating and inhibiting receptors identified patient groups with differing injury characteristics and outcomes. In plasma, patients who developed MODS had significantly higher levels of NK-associated cytotoxic mediators and cytokines. Collectively, these data indicate a specific pattern of hyperacute NK cell activation after major trauma that is characterized by a pattern consistent with cytotoxic lymphocyte activation and is associated with clinical outcome. - Source: PubMed
Publication date: 2026/08/24
Shepherd Joanna MGibb Lucy RTorrance Hew D TManson JoannaPennington Daniel JVulliamy PaulBrohi Karim - Upon recognition of alloantigen, T cells rely on an array of costimulatory and coinhibitory receptors to shape their activation and function. The surface receptor CD43 has been reported to provide myriad functions on T cell related to adhesion, trafficking, and intracellular signaling. We investigated the role of CD43 on CD8 T cells in vitro and in a fully allogeneic model of acute allograft rejection. Following polyclonal activation, CD43 did not impact the initial proliferation of CD8 T cells, although CD43 deficient CD8 T cells had mildly enhanced expression of IL-2Rα and PD-1 relative to CD43 wild-type CD8 T cells (***p = 0.0008 and **p = 0.006, respectively). Following 7-9 days of in vitro culture, CD43 deficient CD8 T cells had a stronger effector phenotype, displaying greater expression of Granzyme B, CD69, IL-2Rα, and PD-1. Following fully allogeneic skin grafting, alloantigen-specific CD43 deficient CD8 T cells accumulated at greater numbers in the secondary lymphoid tissue and the allograft relative to CD43 wild-type CD8 T cells (draining lymph nodes ***p = 0.007, spleen *p = 0.03). Hierarchical clustering and manual gating of revealed that CD43 deficient had an elevated frequency of effector populations with a CD62L, KLRG-1, and CD49d phenotype, and that CD43 KO CD49d cells preferentially infiltrated the allograft tissue (***p = 0.0001). Together, these data provide evidence that CD43 acts as a checkpoint of alloantigen-specific CD8 T cell differentiation after transplantation. - Source: PubMed
Publication date: 2026/09/24
Tang YukaiFreibaum Joel SCohen Gregory SLeathem Riley PKrummey Scott M - Growing evidence highlights the lung -brain axis as a key contributor to CNS autoimmunity. However, accurate characterization of lung immune cells remains technically challenging because standard transcardial perfusion does not eliminate the lung's extensive marginated intravascular leukocyte pool, allowing circulating cells to contaminate analyses of the lung parenchyma. - Source: PubMed
Publication date: 2026/09/09
Azizi GholamrezaRostami Abdolmohamad - Small extracellular vesicles (sEVs) released by infected cells carry microbial antigens together with host immunomodulatory molecules, yet whether their structural integrity governs the durability of protective immunity is unknown. Using infection as a model, we show that sEVs isolated from infected macrophages act as potent antigen carriers for intranasal immunization. In BALB/c mice, intact sEVs elicited antigen-specific serum IgG responses comparable in magnitude to those induced by live attenuated Δ Immunization further increased fecal IgA binding to following lethal challenge and generated serum capable of enhancing macrophage-mediated bacterial uptake. Single-cell RNA sequencing of mesenteric lymph nodes revealed enrichment of mature B cells, effector CD8 T cells, and central memory-like CD4 T cells expressing CD69, CD44, CCR7, and Sell/CD62L, while defined recombinant sEV-associated antigens drove IFN-γ and IL-2 production by memory T cells ex vivo. Disrupting vesicle architecture by sonication left total IgG and IgG1 induction intact but selectively impaired IgG2a responses and antigen-specific T-cell recall; intact sEVs, by contrast, drove greater dendritic-cell CD80 expression, IL-2 production by cocultured CD69+ CD4 T cells, and prolonged survival after lethal challenge. These findings establish that vesicle integrity is dispensable for the overall magnitude of antibody induction but is required to instruct dendritic-cell costimulation, Th1-associated IgG2a class switching, and durable memory T-cell recall after mucosal immunization, identifying infection-derived sEVs as structurally organized immunogens rather than passive antigen reservoirs. - Source: PubMed
Publication date: 2026/09/14
Bhimani SaloniSchultz Alexander CTanaka SaeFerraro Mariola J - Class II lupus nephritis (LN) is considered clinically benign, yet up to 50% of patients progress to more severe disease and no molecular characterization exists. We aimed to define the single-cell landscape of Class II LN and identify cellular and transcriptional features associated with kidney outcome. - Source: PubMed
Publication date: 2026/09/18
Shwetar Jasmine JFava AndreaKeegan SarahCarlucci Philip MDudley Jeffrey NLama LodoeSuryawanshi HemantMorozov PavelMullins Briana JAmarnani AbhimanyuProcell LindaAnnuar DaniaGurajala SiddarthIzmirly Peter MJames Judith AGuthridge Joel MEisenhaure Thomas MArazi ArnonPutterman ChaimRao Deepak ADiamond BettyBelmont H MichaelApruzzese WilliamDavidson AnneRaychaudhuri SoumyaHacohen NirDall'Era MariaLoomis CindyClancy Robert MTuschl ThomasWu MingFine Derek MAtta Mohamed GMonroy-Trujillo JoseFurie RichardKamen Diane LKalunian Kenneth Petri MichelleBuyon Jill PRovin Brad HRuggles Kelly V