CD55
- Known as:
- CD55
- Catalog number:
- 11-230-C025
- Product Quantity:
- 0.025 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD55
Related genes to: CD55
- Gene:
- CD55 NIH gene
- Name:
- CD55 molecule (Cromer blood group)
- Previous symbol:
- DAF
- Synonyms:
- CR, TC, CROM
- Chromosome:
- 1q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
Related products to: CD55
Related articles to: CD55
- Natural killer (NK) cells are central to antitumor immunity but rapidly lose function in the tumor microenvironment (TME). Here, we identify CD55, previously recognized as a complement regulatory protein, as an inducible membrane organizer that coordinates activating receptor signaling to potentiate NK cell-mediated antitumor responses. Upon initial tumor encounter, NK cells upregulate CD55 via an NKG2D-p65 transcriptional axis. Unlike in T-cells, where it has a known co-stimulatory role, CD55 on NK cells directly engages tumor-expressed CD97 in trans to trigger lipid raft aggregation and LCK activation, acting as a self-sufficient primary signal initiator that drives cytotoxicity. However, upon prolonged tumor exposure, CD55 expression on NK cells progressively declines, coinciding with the well‑recognized downregulation of NKG2D upon chronic exposure. Within the TME, this loss of CD55 causally impairs NK-cell function. In cancer patients, low CD55 expression in tumor-infiltrating NK cells correlates with poor clinical outcomes. Restoring CD55 expression in both conventional and chimeric antigen receptor-engineered NK cells augments LCK signaling, enhances effector function and persistence, and improves antitumor efficacy in vivo. Thus, NK cells deploy a CD55-dependent autonomous activation mechanism upon tumor encounter, whereas chronic exposure drives CD55 loss and functional dysfunction, a state that can be therapeutically reversed by CD55 restoration. - Source: PubMed
Publication date: 2026/09/04
Li LingyuLi ZhaozhiLiu YangFan WeiLei YuhongTian LeiChen LichaoQu ZhihuanShi YuanyuanYu JianhuaWang Yufeng - The immunobiology of Guillain-Barré syndrome (GBS) has long been organized around a dichotomy: acute motor axonal neuropathy (AMAN) is an antibody-mediated nodal disorder, whereas acute inflammatory demyelinating polyneuropathy (AIDP) has been interpreted mainly through T-cell-mediated models of compact-myelin injury. Four successive findings challenge this separation. Intraneural injection of GBS sera produced demyelination without transfer of immune cells; pathological studies in AIDP localized complement activation to the Schwann-cell surface before macrophage-associated myelin stripping. Serum IgG from a substantial subset of patients with AIDP bound nodal or paranodal surface domains; and identification of gelsolin-3 defined an AIDP subset in which patient IgG, together with active complement, produced nodal disruption before internodal demyelination. Peripheral-myelin-reactive T cells further indicate that T-cell-mediated and antibody-mediated immunity may coexist. Within this evidence hierarchy, AMAN and a subset of AIDP have distinct initiating targets but converge on nodal dysfunction. CD55 and CD59 are membrane-bound complement regulators: CD55 limits complement amplification, whereas CD59 prevents assembly of the membrane attack complex. Both are detectable in compact myelin but not at human nodes of Ranvier, revealing a localized discontinuity in complement control. This local absence of complement regulators may influence whether antibody binding progresses to conduction failure, axonal degeneration, or internodal demyelination, but should be regarded as a permissive substrate for injury rather than as evidence of lesion localization. Observations in chronic inflammatory demyelinating polyneuropathy (CIDP) suggest that antibody-mediated functional injury may precede structural demyelination. This Review proposes complement-regulated nodal vulnerability to integrate evidence across AMAN and subsets of AIDP and CIDP while preserving differences in targets, tempo, and mechanistic strength. - Source: PubMed
Yuki Nobuhiro - Acute-on-chronic liver failure (ACLF) is a fatal syndrome defined by hepatic decompensation and systemic inflammation, yet the underlying cellular networks remain elusive. Here, we established an ACLF mouse model recapitulating clinical hallmarks and performed single-cell RNA sequencing (scRNA-seq) on hepatic non-parenchymal cells (NPCs). We identified 30 cell clusters and observed profound spatial remodeling of NPCs driven by pro-inflammatory mediators. Endothelial cells (ECs) underwent a critical transition from homeostasis to dysfunction, marked by mitochondrial damage and activation of NF-κB and MAPK pathways. Ligand-receptor interactome analysis identified dysfunctional ECs as central hubs driving global network reconfiguration, primarily via the Lgals9-Ighm/Cd45/Cd44 axes, alongside the suppression of homeostatic signals (Cd55 and APP). Furthermore, we mapped B cell lineage trajectories and validated the spatial co-localization of EC and B-cell interactions through Lgals9-Ighm. This study defines the EC and B-cell communication landscape and suggests that the Lgals9-Ighm axis may play a critical role in ACLF progression, representing a potential candidate for therapeutic intervention. - Source: PubMed
Jia JieDong YuehongZhao YuLi ShaoyouMou Tangwei - Red blood cell (RBC)-camouflaged nanocarriers provide a biomimetic strategy to reduce immune clearance and improve tumour-directed drug delivery. Here, we engineered an RBC-camouflaged albumin nanoplatform co-loaded with oxaliplatin (Oxa) and zinc oxide nanoparticles (nZnO), termed C-Alb, for colorectal cancer therapy. The optimized formulation exhibited a uniform hydrodynamic size of 139.3 ± 2.5 nm, a zeta potential of -17.6 ± 2.3 mV, efficient Oxa/nZnO loading, good colloidal stability, and pH-responsive Oxa/Zn release, with enhanced release under acidic/reductive tumour-mimicking conditions. RBC membrane cloaking preserved vesicular morphology and key membrane-associated components, including glycoproteins, sialic acid, CD47, CD55, and CD59, while reducing macrophage uptake. In CT26 cells, C-Alb enhanced cytotoxicity (IC₅₀ = 4.27 μM), increased caspase 3/7 activation, and induced ICD-associated calreticulin exposure, ATP secretion, and HMGB1 release. These responses promoted M1 macrophage polarization, dendritic cells maturation, and macrophage-mediated phagocytosis of treated tumour cells. The formulation also downregulated CD44 and reduced CT26 adhesion and migration. In CT26 tumour-bearing mice, RBC coating prolonged systemic exposure, reduced RES-associated accumulation, enhanced tumour Oxa deposition, improved antitumour efficacy, and maintained acceptable systemic tolerability. Therefore, C-Alb integrates immune-evasive delivery, Oxa/nZnO co-delivery, ICD-associated immune activation, and improved in vivo antitumour performance. - Source: PubMed
Publication date: 2026/08/27
Hamdi MohamedAbdel-Bar Hend MohamedElmowafy EnasElKashlan Akram MMansour MaiAl-Jamal Khuloud TAwad Gehanne A S - Next-generation sequencing (NGS) is currently regarded as a preferable method for detection of actionable alterations in non-small cell lung carcinomas (NSCLCs). RNA-based NGS is particularly efficient in detection of gene fusions and allows for mRNA expression analysis of relevant genes. This study describes a novel library preparation pipeline for targeted RNA sequencing, which is based on the 5' rapid amplification of the cDNA ends (5' RACE) and anchored multiplex PCR. The NGS panel was designed for the analysis of 15 genes relevant to NSCLC therapeutic decisions (, , (), , (), , , , , , and ). The validation against PCR was performed for 168 NSCLC samples. The NGS assay successfully detected all 85 mutations previously identified by PCR. It also confirmed the absence of tested mutations in 82 out of 83 PCR-negative samples. The only discordant case was subsequently analyzed by digital droplet PCR and demonstrated low fraction of the mutated allele. The newly designed NGS panel was subsequently used for the analysis of 272 carcinomas from young (≤50 years old) patients with no driver mutations identified by PCR tests or with failed PCR analysis. NGS was successful in 240 (88.2%) cases, including 35 (64.8%) PCR-failed samples. Driver mutations were detected in 55 tumors, including three previously unreported fusions (, and ). We conclude that 5' RACE-based RNA sequencing is a viable approach for NSCLC molecular testing. - Source: PubMed
Publication date: 2026/08/13
Mitiushkina Natalia VPreobrazhenskaya Elena VRomanko Aleksandr AShestakova Anna DBelova Rimma SVelyukhova Tatiana YTretyakova Yana IFirsova Natalia ANalivalkina Ekaterina ATiurin Vladislav IImyanitov Evgeny N