Ask about this productRelated genes to: CD69 antibody
- 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 antibody
Related articles to: CD69 antibody
- The mechanisms underlying compensatory renal hypertrophy (CRH) in living kidney donors after unilateral nephrectomy (UNx) remain complex and underexplored. We examined immune cells involved in CRH after UNx in mice. Following UNx of the left kidney in WT mice, GFR measurements, flow cytometry, and single-cell RNA sequencing were performed over 8 weeks. Rag1 mice were studied to explore role of adaptive immune cells in GFR changes during CRH. Immune cells showed dynamic, time-dependent changes after UNx. Innate immune system responded rapidly, with increases in neutrophils and macrophages, while NK cells initially decreased. Subsequently, adaptive immune cells, including CD4⁺, CD8⁺, and DN-T cells, showed changes in resident marker CD69 and regulatory markers such as CD4⁺CD25⁺. Expression of PD-1, CTLA-4, and TIGIT on T cells changed during acute injury (0-24 hours), recovery phase (24 hours-1 week), and immune remodeling (4-8 weeks). GFR was significantly higher in later recovery phase in Rag1 mice than in WT. These findings demonstrate multi-phase immune cell changes in remnant kidney after UNx, characterized by rapid innate immune cell activation, gradual adaptive immune cell regulation, and shifts in immune checkpoint levels. These immune changes could influence compensatory changes, including GFR in live kidney donors and others after UNx. - Source: PubMed
Publication date: 2026/05/15
Patel Shishir KumarGuo QisenGooya MahtaMatsuura RyoJung Hyun JunKapoor RadhikaRastegar Tara FallahNoel SanjeevRabb Hamid - T cells drive post-stroke secondary brain injury, with the Th17/Treg balance shaping post-stroke inflammation. Soraphen A (SorA) inhibits Th17 polarization while preserving Tregs. We examined SorA's effects on post-stroke T cell activation - distinguishing antigen-specific from bystander activation - including inflammatory conditions induced by LPS. - Source: PubMed
Publication date: 2026/05/08
Gellrich JulianeBödecker NoraReich ImkeRuhnau JohannaGroß StefanKirsch Susanne HMüller RolfSchulze JulianeVogelgesang Antje - Tissue-resident memory T (T) cells have become a paradigm shift in the field of immunology and have changed our view of local immune surveillance at barrier surfaces. In contrast to circulating memory T cells, T cells are fixed in non-lymphoid organs like lungs, intestine and skin to act as the first line of defense against reinfection and malignant conversion. The finding contradicts the conventional emphasis on exercise immunology on the number of circulating lymphocytes and requires a new conceptual framework of the so-called quantitative to spatial immune remodeling. This review summarizes the current developments in the T cell biology and its relevance to exercise immunology and answer the main question of the review: will endurance training, like a vaccine, elevate the density of both T cells in non-lymphoid tissues and their functional capacity? To begin with, we define the molecular basis of T cells, their differentiation routes, storage processes (CD69, CD103), and tissue-specific diversity. Then, we explore the possible ways in which exercise might be able to change the establishment of T cells and their functions, namely exercise related adrenergic signaling, thermoregulatory shifts, and hemodynamic forces regulating the T cell homing receptor and tissue resident program. The traditional finding of decreased upper respiratory tract infection risk in athletes is reevaluated based on the perspective of increased respiratory mucosal T cell immunity. We then elaborate on the biphasic J-shaped relationship between exercise intensity and immunoprotection, and elucidate how optimal training levels are achieved at lower intensities whereas higher intensities can undermine the level of T cell-mediated immunity. Lastly, we have identified key knowledge gaps and research directions that are needed in the future, namely, the mechanistic analysis of β2-adrenergic receptor signaling in T cell biology, the creation of tissue-specific exercise prescription strategies and the translation of these findings into practice as a way to prevent infections and treat cancer immunotherapy. Incorporating basic immunology with exercise physiology, the review is intended to trigger a paradigm shift in exercise immunology shifting away the circulating numbers toward the spatially-resolved insight of how exercise alters the immune picture of the tissues. - Source: PubMed
Publication date: 2026/05/07
Xie EnliHe YushanCao TainanLi ChangchunWang Zhiming - Crohn's disease is biologically heterogeneous, and current clinical classifications poorly predict treatment response or disease progression. The molecular programs that drive clinical outcomes in Crohn's disease remain poorly defined. We generated and analyzed whole-transcriptome RNA-sequencing data from non-inflamed colonic biopsies of 101 well-characterized Crohn's disease patients. We performed weighted gene co-expression network analysis and identified 15 transcriptional programs that stratified Crohn's disease independent of conventional clinical classification. We then tested associations between these programs and clinical outcomes, including primary and secondary treatment failure, surgical burden, and perianal disease. A neutrophil activation program enriched for CD69 expression was strongly associated with both primary and secondary treatment failure, identifying a mucosal immune phenotype of therapeutic resistance. A fibro-proliferative program centered on SERPINE1 expression correlated with higher cumulative surgical burden, implicating tissue remodeling pathways in progressive disease. We also discovered an antimicrobial program, marked by elevated DEFA5 and DEFA6, in colonic mucosa; this signature was enriched in patients with treatment failure and validated by DEFA5 immunofluorescence. A distinct program uniquely associated with perianal disease highlights the molecular features of this severe phenotype that are not captured by standard clinical metrics. In conclusion, colonic transcriptional programs identify biologically meaningful disease states in Crohn's disease that associate with treatment failure, surgical risk, and perianal involvement. These findings provide a molecular basis for prognostic biomarkers and targeted therapeutic stratification in Crohn's disease. - Source: PubMed
Publication date: 2026/05/19
Awad AyeshHuan BenjaminShanahan Michael TWeaver DavidSilverstein SophieLau GwenLian GraceFurey BradyMcMichael Benjamin DArias AntonioKeith Benjamin PShumway Alexandria JSethupathy PraveenFurey Terrence SSheikh Shehzad Z - Dendritic cells (DCs) play a pivotal role in initiating robust T cell responses against tumors, yet effective strategies to enhance DC activation remain limited. This study explores the synergistic effects of Lycium barbarum polysaccharide (LBP) and the tumor cell lysate of endothelial progenitor cells (EPC-TCL) to boost DC activation and anti-tumor immunity. Using flow cytometry, the enzyme-linked immunosorbent assay, western blot analysis, and in vivo tumor models, we demonstrate that the combination treatment significantly enhanced expression of co-stimulatory molecules (CD40, CD80, CD86, and MHC-I) in DCs and elevated cytokine levels (IL-6 and IL-12). Co-culture experiments revealed that T cells primed with LBP and EPC-TCL-modified DCs increased proliferation and reduced exhaustion, characterized by upregulated CD69 and downregulated PD-1. Mechanistically, activation of the MAPK and STING signaling pathways was confirmed by phosphorylation of key proteins. Moreover, T cells activated by DCs treated with LBP and EPC-TCL exhibited potent anti-tumor effects, significantly reducing invasiveness of mouse lung carcinoma cells and impairing angiogenesis in vitro. In a mouse axillary tumor model, the combination treatment markedly suppressed tumor growth and induced apoptosis of tumor cells. These findings highlight the potential of LBP and EPC-TCL as novel immunotherapeutic agents targeting DCs to enhance anti-tumor immunity. Future studies will focus on clinical validation and integration into combination therapies for broader cancer applications. - Source: PubMed
Publication date: 2026/05/19
Wang LifangWang ZiyeZhu ChangchangChen WenhuZhao Hongguang