Anti-Human CD59 (Protectin) FITC 25 tests
- Known as:
- Antibody toHuman CD59 (Protectin) fluorecein 25 tests
- Catalog number:
- 11-0597-41
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD59 (Protectin) FITC 25 tests
Related genes to: Anti-Human CD59 (Protectin) FITC 25 tests
- Gene:
- CD59 NIH gene
- Name:
- CD59 molecule (CD59 blood group)
- Previous symbol:
- MIC11, MIN1, MSK21, MIN2, MIN3
- Synonyms:
- 16.3A5, EJ16, EJ30, EL32, G344, p18-20
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2019-04-23
Related products to: Anti-Human CD59 (Protectin) FITC 25 tests
Related articles to: Anti-Human CD59 (Protectin) FITC 25 tests
- - Source: PubMed
Publication date: 2026/06/01
Viswanathan VenkataramanNirmalkumar BaalakumarMadhuri Karnati Guna - This report presents the case of a 60-year-old woman who was admitted with symptoms of fatigue and poor appetite. Laboratory investigations revealed severe acute kidney injury (AKI), indicated by a serum creatinine level of 2,065 μmol/L, necessitating the initiation of emergency hemodialysis. The patient also exhibited hemolytic anemia (hemoglobin, 69 g/L), thrombocytopenia (platelet nadir, 45 × 10/L), venous thrombosis, a positive direct antiglobulin test (DAT), and a low absolute reticulocyte count. Conventional flow cytometry (red blood cells and neutrophils CD55/CD59) did not detect a paroxysmal nocturnal hemoglobinuria (PNH) clone. Renal biopsy revealed hemoglobin cast nephropathy and intrarenal venous thrombosis. Subsequent bone marrow evaluation, high-sensitivity flow cytometry (FLAER method), and supportive PIGA sequencing findings established the diagnosis of PNH. Treatment with eculizumab led to hematologic remission and progressive renal recovery. This case underscores the importance of considering PNH in patients with severe AKI and hemolysis, even when initial conventional flow cytometry is negative. - Source: PubMed
Publication date: 2026/05/08
Jiang LuyaoChen TianxiXu LinlinShi MiaojunHuang Wen - Psoriasis is a chronic, immune-mediated inflammatory disease that affects approximately 2%-3% of the global population, and remains a major dermatologic and psychosocial burden. Despite advances in biologics targeting interleukin 17 (IL-17) and interleukin 23 (IL-23) pathways, effective and accessible treatment options for moderate psoriasis are lacking. Topical therapies and phototherapy are often inadequate, while systemic agents and biologics are limited by toxicity, high cost, and restricted reimbursement criteria, leaving patients with moderate disease without adequate therapeutic options. Mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) have emerged as a promising acellular therapeutic modality that harnesses the immunomodulatory and regenerative properties of parent MSCs. Unlike systemic biologics, MSC-EVs act locally and non-immunosuppressively. Topically applied MSC-EVs have demonstrated the ability to modulate cutaneous inflammation by attenuating complement activation [via CD59-mediated inhibition of complement terminal component 5b-9 (C5b-9) complex formation], reducing neutrophil infiltration, and subsequently lowering IL-17 and IL-23 expression in psoriatic lesions. Preclinical and early clinical studies suggest that MSC-EVs can restore local immune homeostasis through paracrine extracellular mechanisms, without systemic absorption or adverse effects. MSC-EVs represent a new class of cell-free nanotherapeutics inspired by biologics, capable of localized immunomodulation in psoriasis. By combining biologic-like efficacy with the safety and accessibility of topical therapy, MSC-EVs may bridge the long-standing therapeutic gap in moderate psoriasis. This review discusses current treatment limitations, the mechanistic rationale for MSC-EVs in psoriatic inflammation, and their potential to redefine dermatologic immunotherapy. - Source: PubMed
Publication date: 2026/04/24
Tan Thong TeckTan Kok HianLim Sai Kiang - CD59 is an endogenous complement inhibitor that restricts membrane attack complex formation, protecting cells from complement-dependent cytotoxicity. Dysfunctional CD59 leads to uncontrolled complement activation and contributes to the pathogenesis of various diseases, including neuromyelitis optica spectrum disorder (NMOSD), a rare inflammatory autoimmune disorder specifically targeting astrocytes. However, the mechanisms underlying the regulation of CD59 expression are complex and need to be elucidated. Here, we show that in a clinically relevant NMOSD model using female mice, astrocytic CD59 protects astrocytes from AQP4-IgG and complement-mediated attacks. Through secretome and transcriptome analysis, we identified brain endothelial cell-derived SPARC as an inhibitor of VEGFA/VEGFR2 signaling, which suppresses astrocyte proliferation and CD59 production. Endothelial SPARC loss increases astrocytic CD59 and mitigates autoimmune astrocytopathy, whereas VEGFR2 activation induces CD59 and alleviates disease. Collectively, this study reveals how endothelial SPARC regulates astrocytic CD59 expression, promoting autoimmune astrocytopathy and providing a potential avenue for astrocyte-targeted therapies in NMOSD. - Source: PubMed
Publication date: 2026/05/12
Cui TingtingGong YeWang ZhenLi PeiDai LuhangChen JiaFeng ZheLiu XueliLi ShaogangLiu HuanyiLi KeDing XiaoliXue XiaochangYang LutingZhang LeiLi RuiFu YingZhang YalingYan Yaping - Parkinson's disease (PD) is characterized by progressive degeneration of nigrostriatal dopamine neurons and synucleinopathy, which is the accumulation of aggregated α-synuclein (α-syn). Increasing evidence implicates α-syn-associated neuroinflammation as a contributor to PD pathogenesis; however, immune mechanisms linking synucleinopathy to neurodegeneration remain incompletely defined. Activation of the complement cascade occurs in PD and other neurodegenerative disorders, but most studies report complement activation after overt neurodegeneration, making it difficult to conclude if complement is directly activated by pathological α-syn or secondarily following neurodegeneration. We used the rat α-syn preformed fibril (PFF) mode, complement assays and human postmortem PD tissue to test whether pathological α-syn directly activates complement prior to overt neurodegeneration. The α-syn PFF model exhibits a protracted pathological time course and distinct temporal separation between peak α-syn aggregation and nigrostriatal degeneration; thus we quantified complement expression, activation, and regulation during the aggregation phase. Synucleinopathy induced complement activation prior to nigrostriatal degeneration, including upregulation of components of both the classical ( ) and alternative ( ) pathways, the anaphylatoxin ( ) and phagocytic ( ) complement receptors, and activation of complement C3. During early synucleinopathy, microglia upregulated C3 which significantly correlated with synucleinopathy burden across several brain regions, including the substantia nigra pars compacta (SNc) and cortex. Concurrently, complement regulatory proteins, including CD55, CD59, neuronal pentraxin-1 (Nptx1), and the neuronal pentraxin receptor were downregulated in the synucleinopathy-affected SNc. Importantly, increased levels of C1q and iC3b along with downregulation of CD55 and NPTX1 were also observed in human postmortem PD SNc, supporting the translational relevance of our findings. Mechanistically, we demonstrate that aggregated, but not monomeric, α-syn directly binds C1q and activates the complement cascade in a C1q-dpendent manner. These data provide the first evidence that synucleinopathy triggers complement activation and dysregulation prior to neurodegeneration. - Source: PubMed
Publication date: 2026/04/30
Khan HinaGifford MaryKordbacheh ArashBury AsherPanoushek SpencerCole-Strauss AllysonKemp Christopher JLuk Kelvin CSteece-Collier KathyKuhn Nathan CKanaan Nicholas MSortwell Caryl EPatterson Joseph RBenskey Matthew J