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
- Idiopathic aplastic anaemia (AA) is a life-threatening autoimmune bone marrow (BM) failure syndrome characterized by a hypocellular BM and peripheral pancytopenia. While dysregulation of the complement system has been implicated in the pathogenesis of several autoimmune diseases, including rheumatoid arthritis and systemic lupus erythematosus, its role in AA remains poorly understood. Notably, autoantibodies are frequently detected in AA patients and have the potential to activate the complement cascade. Using an immune-mediated murine model of AA, we found that allogeneic transplantation of splenocytes induced BM failure accompanied by activation of the complement system, as evidenced by elevated plasma levels of complement components C3 and C5. To functionally dissect the contributions of direct cytotoxic T-cell effects versus indirect mechanisms such as complement activation, we co-transplanted hematopoietic stem and progenitor cells (HSPCs) congenic to the donor splenocytes into allogeneic recipient mice. In this context, HSPCs deficient in the complement inhibitor Cd55 were negatively selected, indicating increased susceptibility to complement-mediated attack in vivo. Importantly, pharmacological inhibition of the complement cascade rescued the selective disadvantage of Cd55-deficient HSPCs in AA mice, demonstrating that complement activation imposes a negative selective pressure on HSPCs in this model. Together, these findings support a functional role for the complement pathway in the pathogenesis of immune-mediated AA. Further studies are warranted to evaluate the therapeutic potential of combining complement inhibition with standard immunosuppressive therapy in patients with AA. - Source: PubMed
Publication date: 2026/08/20
Kalampalika FoteiniSanchez-Lanzas RaulJimenez-Pompa AmandaHateley AbigailGanuza Miguel - CD4+ T cell dysfunction plays a critical role in the pathogenesis of rheumatoid arthritis (RA). In this study, we investigated the expression, phenotypic characteristics, and potential clinical significance of CD55, a membrane-bound complement regulatory protein, in peripheral blood CD4+ T cells from RA patients. Flow cytometric analysis revealed that CD55 expression was highest in naive CD4+ T cells and was significantly reduced in patients with early RA compared with healthy controls. Functionally, CD55+CD4+ T cells displayed enhanced production of IL-17, IL-21, and IL-22 following stimulation and exhibited reduced susceptibility to complement deposition. Transcriptomic analysis identified distinct molecular signatures associated with CD55 expression, which were further validated at the protein level, including increased expression of PAX5, CR2, and CD248 in CD55+CD4+ T cells. In addition, CD55 expression was inversely associated with p38 MAPK activation, suggesting a link between CD55 downregulation and aberrant T cell activation. Receiver operating characteristic analysis demonstrated that CD55+CD4+ T cell frequency possessed diagnostic value for distinguishing patients with early RA from healthy controls and primary Sjögren's syndrome patients. Collectively, these findings identify CD55 as a marker of a distinct CD4+ T cell subset with altered functional and molecular characteristics and support its potential utility in the early diagnosis and differential diagnosis of RA. - Source: PubMed
Bahabayi AyibaotaGao YimingXiong ZiqiSun XiaochenLi QiZhang ZhonghuiWang GuochongLiu Chen - CHAPLE syndrome is an ultra-rare genetic cause of protein-losing enteropathy (PLE) resulting from uncontrolled complement activation due to CD55 deficiency. We report two paediatric patients presenting with recurrent diarrhoea, hypoalbuminaemia, hypogammaglobulinaemia and growth failure, both initially evaluated as intestinal lymphangiectasia. Persistent symptoms and poor response to conventional therapy prompted genetic evaluation, which revealed pathogenic variants in the CD55 gene in both children, confirming the diagnosis of CHAPLE syndrome. Both patients required repeated albumin and intravenous immunoglobulin replacement prior to diagnosis. Targeted therapy with pozelimab was initiated. Rapid clinical and biochemical improvement was observed within 2 weeks, with sustained normalisation of albumin, total protein and immunoglobulin levels. At 3-month follow-up, both children remained in clinical remission without further need for albumin or immunoglobulin infusions. These cases highlight the importance of considering genetic causes in children with refractory PLE and demonstrate the effectiveness of early targeted complement inhibition in CHAPLE syndrome. - Source: PubMed
Publication date: 2026/08/17
Grotra RohanBhadani HimanshuMalik Rohan - A strong crosstalk exists between endoplasmic reticulum (ER) stress and synovitis. Beyond their canonical role in protein folding, ER stress chaperones may promote inflammation, cell survival, and fibroblast activation under pathological conditions. This study aimed at localizing and quantifying 11 ER stress proteins (BiP, HYOU1, MANF, PDIA4, GANAB, HSP90B1, TXNDC5, DNAJB11, LMAN1, ERP29, CALR) in human inflamed synovial membranes and at investigating their expression in fibroblast-like synoviocytes (FLS) under ER stress, pro-inflammatory, or pro-fibrotic stimuli. By immunohistochemistry, on a first cohort of formalin-fixed paraffin-embedded (FFPE) biopsies obtained from patients with osteoarthritis (OA), chronic pyrophosphate arthropathy (CPPA), and rheumatoid arthritis (RA), these ER chaperones were primarily localized to the lining in low-grade inflammation (Tak <4) and expanded to the sublining under high inflammatory conditions (Tak ≥4), with a widespread distribution in RA. Imaging mass cytometry, applied to a second cohort of FFPE tissue samples collected from patients diagnosed with OA and RA, revealed the co-expression of ER stress proteins with CD55⁺ FLS in the lining and their progressive infiltration into the sublining along with CD34⁺CD31 FLS during inflammation. These observations were confirmed by immunofluorescence on a larger cohort of OA patients. As inflammation progresses, there is a loss of co-expression with CD55 in the lining, accompanied by a gradual shift towards co-expression with CD34 in the sublining. In vitro, ER stress proteins, particularly BiP, HYOU1, MANF, PDIA4, HSP90B1, LMAN1, CALR, and DNAJB11 are overexpressed in human OA FLS following ER stress, pro-inflammatory or pro-fibrotic stimulation, with BiP, PDIA4, HSP90B1, ERP29, and CALR also being secreted. PDIA4 emerged as a central player: its depletion significantly impaired FLS proliferation and migration, highlighting a direct role in driving synovitis. This study provides the first spatial and functional characterization of ER chaperones in human arthritic synovium, linking ER stress to fibroblast plasticity, inflammation, and fibrosis. - Source: PubMed
Publication date: 2026/08/12
Gendebien ZoéPoulet ChristopheDeroyer CélinePaulissen GenevièveSalpetier PaulineHego AlexandreLefèvre GaëtanCobraiville GaëlNeuville SophiePlener ZeldaDaniel ChristopheThirion ThierrySokolova TatianaDurez PatrickHemon PatriceDelarue YunaMarec NadègeBianchi ElettraDelvenne PhilippeRibbens Cliode Seny Dominique - Red blood cell (RBC)-based therapeutic enzyme delivery systems require cell sources that can support future standardized large-scale production, with the prerequisite that engineering modifications preserve the cells' inherent biocompatibility and long-circulating potential. In this study, we first demonstrated proof-of-principle by successfully engineering asparaginase (ASPG)-loaded erythroid cells in the human erythroid progenitor cell line (HUDEP-2), where efficient ASPG expression and intact enzymatic activity were confirmed. To facilitate clinical translation, the validated strategy was further applied to human induced pluripotent stem cells (iPSCs), and the differentiated products were systematically characterized. It is worth noting that the key membrane markers of iPSC-derived ASPG-loaded erythroid cells (i-ASPG-R), including CD47 and CD55, were comparable to those of human RBCs (hRBCs). The results of Annexin V staining indicated a healthy cell status. More importantly, these cells displayed ASPG activity equivalent to that of HUDEP-2-derived counterparts. Moreover, the expression of ASPG did not affect enucleation and the composition of globin. In vitro function assays showed that compared with the control group, the proliferation of CCRF-CEM leukemia cells was inhibited by 48% after 24 h of co-culture with i-ASPG-R. In summary, this study established an iPSC-derived platform for generating ASPG-loaded erythroid cells with favorable carrier properties and evident anti-leukemic activity in vitro, laying a conceptual foundation for future cell therapy manufacturing via optimized terminal maturation. - Source: PubMed
Publication date: 2026/08/08
Cheng XiaobeiZhang BiaoLing YamengDeng HuiziYang YangXi JiafeiYang MeiyanGong WeiWang YuliYue WenLi YiGao Chunsheng