Ask about this productRelated genes to: CD44 antibody
- Gene:
- CD44 NIH gene
- Name:
- CD44 molecule (Indian blood group)
- Previous symbol:
- MIC4, MDU2, MDU3
- Synonyms:
- IN, MC56, Pgp1, CD44R, HCELL, CSPG8
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: CD44 antibody
Related articles to: CD44 antibody
- Resident memory T cells (Trm) are key mediators of protective immunity at barrier sites, yet their development during early life remains poorly defined. Here, we show that early-life oral vaccination with a heterologous rhesus rotavirus (RV) induces short-lived intestinal Trm that are negative by intravascular staining and express a CD44+CD69+CD103+/-P2X7R+ phenotype. Blocking lymphocyte homing with an anti-α4β7 antibody during vaccination did not alter the magnitude of RV-specific intestinal T cells or affect protection following murine RV challenge. In contrast, reduction of RV-specific intraepithelial lymphocytes by nicotinamide adenine dinucleotide treatment, or genetic deletion of the aryl hydrocarbon receptor repressor (Ahrr-/- mice)-which also exhibit decreased intraepithelial CD8+ T cells after infection-resulted in increased viral antigen shedding upon challenge. These results suggest that intestinal Trm cells induced by early-life vaccination may contribute to protection against RV infection. - Source: PubMed
Publication date: 2026/06/13
Montenegro CatherineRondón Martín AlonsoDing SiyuanPerdomo-Celis FedericoFranco Manuel A - Microglia, the immune cells of the central nervous system (CNS), quickly respond to neurodegeneration by proliferating and migrating to areas of disease, phagocytosing debris, and releasing cytokines to initiate inflammation. Critically, the mechanisms underlying these microglial functions remain only partly understood. One molecular regulator of interest is complement protein C1q, the initiator molecule of the complement cascade that increases 300-fold in healthy aging and accumulates with neurodegeneration. We have previously reported that exogenous C1q treatment alters inflammatory gene expression and cell function in human induced pluripotent stem cell-derived microglia (iMG). Here, we test the hypothesis that C1q induced cell changes are modulated by novel C1q receptor, CD44. We first confirmed expression of five novel C1q receptors at the RNA and protein levels, and then validated C1q-receptor binding on the iMG cell surface using proximity ligation assay. Based on these results, we selected CD44 as an initial target and generated CD44 knockout iMG to test the role of CD44 in the iMG response to C1q. We demonstrate that C1q-CD44 interactions regulate changes in microglial phagocytosis, proliferation, and migration. These data suggest C1q interacts with CD44 to modulate microglial functions that are critical to health and disease, thus informing future directions to test whether these interactions are altered in neurodegenerative disease. - Source: PubMed
Publication date: 2026/06/12
Sakthivel Pooja SVillegas Alyssa JLakatos AnitaKaipa MeghanaLopez Julian MLing AshleyElrachid Zeina HKaram JoshAnderson Aileen J - Tumour-draining lymph nodes (TDLNs) serve as the closest immunological hubs to the primary tumour site in colorectal cancer (CRC). Owing to their unique and irreplaceable anatomical advantage and dynamic immune cell repertoire, TDLNs represent an intensively studied immunological niche and are a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/12
Wang JianZhou MingTan BorenShi HaoyuLiu LeiXu XiaomingGe XiaoxuYang GuanliSheng BiaoHe XianguiLi JunWu Jingjing - The malignant progression of bladder cancer is closely linked to the tumor microenvironment, yet the role of urine-derived stem cells (USCs) remains poorly understood. USCs were isolated from healthy individuals and bladder cancer patients, followed by multi-omic and functional characterization. The bladder cancer cell line T24 was used for in vitro co-culture and in vivo co-injection assays. Sustained exposure to tumor-derived factors (TNF-α, IL-6, and TGF-β) reprogrammed normal USCs (N-USCs) into tumor-associated USCs (T-USCs). This transition was marked by E-cadherin downregulation, vimentin upregulation, cell cycle arrest, and reduced adhesion, facilitating detachment and shedding of USCs into urine. Consequently, urine from tumor-bearing conditions showed increased USC counts and elevated CXCL2 levels. USC-derived CXCL2 activated the CXCR2 receptor on bladder cancer cells, triggering the ERK/β-catenin axis. This significantly upregulated stemness markers (CD44, ALDH1A1), promoting malignant progression. In a co-injection model, T-USCs and bladder cancer cells formed an organized stromal sheath that facilitated tumor invasion. In vivo, USCs drove tumor growth and microenvironment remodeling, effects suppressed by targeting the CXCL2/CXCR2/ERK axis. We propose a model in which hematogenous tumor factors induce urinary USC reprogramming, potentially establishing a CXCL2-enriched niche that fuels malignancy. These findings suggest a biologically plausible "tumor associated USCs-CXCL2-bladder cancer" circuit, providing insights into a putative blood-urine interactive regulatory axis and revealing a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/12
Sun DongkaiHan ChunhuaLi DanLi PengTian XintaoLiang ZhijuanChen YuanbinWang LipingLi ShuaishuaiSun LijiangLiang YeNiu Haitao - Proteolysis-targeting chimeras (PROTACs) are attractive targeted protein degradation modalities, while their clinical advancement is limited by high molecular weight, suboptimal bioavailability, low cellular permeability, and unsatisfactory in vivo efficacy. Herein, we developed a self-assembled nanoparticle system (PRO NPs) constructed from amphiphilic PROTACs. Owing to their intrinsic amphiphilicity, PRO NPs can spontaneously assemble into stable nanoparticles without external excipients, simplifying fabrication and alleviating carrier-associated toxicity. Compared with the free EGFR-targeting PROTAC, PRO NPs exhibited enhanced aqueous solubility and efficient EGFR degradation in HCC827 cells. In vivo, PRO NPs functionalized with hyaluronic acid (HA) through electrostatic adsorption could actively accumulate at tumor sites via CD44-mediated targeting, exerting potent antitumor efficacy (TGI = 76.8%) with reduced systemic toxicity. Collectively, these findings provide novel insights into nano-PROTAC design and a promising strategy for the development of targeted protein degradation therapies. - Source: PubMed
Publication date: 2026/06/12
Ma JunhuiFang LeiWu YuJiao HuiXiang GuangyaMa Xiang