CD55
- Known as:
- CD55
- Catalog number:
- 11-230-C100
- Product Quantity:
- 0.1 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
- Local expression of complement components in the kidney has been reported sporadically in both diseased and normal kidneys. This study aimed to comprehensively characterize the expression of complement components in human glomerular mesangial cells (GMCs), glomerular endothelial cells (GECs), podocytes, and proximal tubular epithelial cells (PTECs) in non-diseased renal tissue. - Source: PubMed
Publication date: 2026/09/01
Gao YuemingLi QiWang YueDeng Zhenling - Evidence-based, mechanism-guided therapies are urgently needed for treating monogenic inflammatory bowel disease (mIBD). For such rare diseases, mechanistic insight is essential to guide treatment when conventional clinical trials are often not feasible. We aimed to summarize literature-based evidence and to identify knowledge gaps. - Source: PubMed
Yeh Pai-JuiCharlesworth James E GTaylor HenryAshton James JNash KatrinaLam Kin Hangde Ridder LissyVuijk Stephanie AYe ZiqingHuang YingBildstein TaniaHaller WolframJones Kelsey D JShouval Dror SWeiss BatiaLau Yu LungBui-Thi-Thuy QuynhMuise Aleixo MRichards DuncanTravis SimonTurner DanUhlig Holm H - Epidermal growth factor receptor (EGFR) mutations represent a central oncogenic driver in non-small cell lung cancer (NSCLC). While EGFR tyrosine kinase inhibitors (TKIs) have revolutionized the management of NSCLC, acquired resistance remains a major hurdle. In response, antibody-based therapeutic strategies have gained increasing attention as a means to overcome TKI resistance and extend disease control. This review synthesizes the rapidly evolving landscape of antibody-based therapeutics for EGFR-mutant NSCLC. We first summarize the mechanisms of monoclonal antibodies directly targeting EGFR, including cetuximab and necitumumab, and discuss their therapeutic limitations. We then highlight the emergence of bispecific antibodies designed to simultaneously target EGFR and key resistance pathways, such as MET. In addition, we review combination strategies integrating EGFR inhibition with antibodies directed against alternative oncogenic pathways or the tumor microenvironment, including anti-angiogenic agents such as bevacizumab. A major focus of this review is antibody-drug conjugates (ADCs) targeting novel surface antigens, including HER2, HER3, and TROP2. By delivering highly potent cytotoxic payloads selectively to tumor cells, these ADCs have demonstrated remarkable clinical efficacy in EGFR TKI-resistant settings. Furthermore, we examine the complex and evolving role of immunotherapy in EGFR-mutant NSCLC. Beyond immune checkpoint blockade, we discuss emerging immunomodulatory strategies targeting the adenosine pathway (CD73), phagocytosis checkpoints (CD24), and complement regulatory proteins (CD55/CD59). Finally, we explore advanced antibody modalities, including immune-engaging bispecific antibodies and next-generation ADCs. Collectively, antibody-based therapies are reshaping the treatment landscape through diverse mechanisms, offering renewed promise for overcoming resistance and improving outcomes in EGFR-mutant NSCLC. - Source: PubMed
Publication date: 2026/09/11
Chen XinranLiang JiaqiZhu JunkanHuang XiaolongHu YiduLin ZongwuZhan Cheng - 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