Expression of CD55 and CD59 on peripheral blood cells from systemic lupus erythematosus (SLE) patients

Alegretti, Ana Paula; Mucenic, Tamara; Merzoni, Jóice; Faulhaber, Gustavo Adolpho Moreira; Silla, Lúcia Mariano da Rocha; Xavier, Ricardo Machado

doi:10.1016/j.cellimm.2010.07.013

Cited by 36 publications

(26 citation statements)

References 26 publications

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“…Tsunoda et al [20] found that the proportion of CD59 on activated T CD8+ lymphocytes in SLE patients was significantly reduced compared to controls and that it could be correlated with disease activity and to be involved in the induced apoptosis of these cells. Our data showed that the decreased expression was unrelated to disease activity and accumulated damage using SLEDAI and SLICC, as has been reported [19, 21], but demonstrated that the lower the C3 level and consequently the greater complement activation, the lower the expression of CD55 on lymphocytes in these patients.…”

Section: Discussionsupporting

confidence: 87%

“…We have previously reported a decreased expression of CD55 (but not of CD59) on neutrophils from SLE patients [21], and decreased CD35 expression on neutrophils has also been shown [16, 25]. In this study, beside confirming the decreased expression of CD55 and CD59, it was demonstrated that the higher the disease activity, the lower their expression on neutrophils.…”

Section: Discussionsupporting

confidence: 84%

“…Particularly, altered expression on blood cells could be related to cytopenic changes common in this disease. Earlier studies have shown that expression of CD35 [12–16], CD55, and CD59 [17, 18] on erythrocytes and CD55 and CD59 [19–21] on lymphocytes are decreased in patients with SLE, but some of these findings were controversial. The current study aimed to evaluate the expression of CD55, CD59, CD46, and CD35 expression on peripheral blood cells from SLE and healthy controls using flow cytometry and its correlation with cytopenias on these patients.…”

Section: Introductionmentioning

confidence: 99%

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Diminished Expression of Complement Regulatory Proteins on Peripheral Blood Cells from Systemic Lupus Erythematosus Patients

Alegretti

Schneider

Piccoli

et al. 2012

Clinical and Developmental Immunology

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CD55, CD59, CD46, and CD35 are proteins with complement regulatory (Creg) properties that ensure cell and tissue integrity when this system is activated. The aim of this study was to evaluate the Creg expression on peripheral blood cells from SLE patients and its association with cytopenia and disease activity. Flow cytometric analyses were performed on blood cells from 100 SLE patients and 61 healthy controls. Compared with healthy controls, we observed in SLE patients with lymphopenia and neutropenia decreased expression of CD55, CD59, and CD46 (P < 0.05). In SLE patients with anemia, CD59 and CD35 were decreased on red blood cells. Furthermore, there was a negative correlation between CD55 and CD59 on neutrophils and the disease activity. The results suggest there is an altered pattern of Creg expression on the peripheral blood cells of SLE patients, and the expression is correlated with disease activity and/or with activation of the complement system.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 84%

Section: Introductionmentioning

confidence: 99%

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Diminished Expression of Complement Regulatory Proteins on Peripheral Blood Cells from Systemic Lupus Erythematosus Patients

Alegretti

Schneider

Piccoli

et al. 2012

Clinical and Developmental Immunology

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“…CD59 are glycosylphosphatidylinositol-anchored proteins with complement inhibitory properties that prevent the terminal polymerization of the membrane attack complex. Increased numbers of CD55- and CD59-lymphocytes and CD59-granulocytes were found in SLE patients as compared with controls (9). …”

Section: Resultsmentioning

confidence: 99%

Bioinformatics Analysis of the Factors Controlling Type I IFN Gene Expression in Autoimmune Disease and Virus-Induced Immunity

Feng

Barnes

2013

Front. Immunol.

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Patients with systemic lupus erythematosus (SLE) and Sjögren’s syndrome (SS) display increased levels of type I interferon (IFN)-induced genes. Plasmacytoid dendritic cells (PDCs) are natural interferon producing cells and considered to be a primary source of IFN-α in these two diseases. Differential expression patterns of type I IFN-inducible transcripts can be found in different immune cell subsets and in patients with both active and inactive autoimmune disease. A type I IFN gene signature generally consists of three groups of IFN-induced genes – those regulated in response to virus-induced type I IFN, those regulated by the IFN-induced mitogen-activated protein kinase/extracellular-regulated kinase (MAPK/ERK) pathway, and those by the IFN-induced phosphoinositide-3 kinase (PI-3K) pathway. These three groups of type I IFN-regulated genes control important cellular processes such as apoptosis, survival, adhesion, and chemotaxis, that when dysregulated, contribute to autoimmunity. With the recent generation of large datasets in the public domain from next-generation sequencing and DNA microarray experiments, one can perform detailed analyses of cell-type specific gene signatures as well as identify distinct transcription factors (TFs) that differentially regulate these gene signatures. We have performed bioinformatics analysis of data in the public domain and experimental data from our lab to gain insight into the regulation of type I IFN gene expression. We have found that the genetic landscape of the IFNA and IFNB genes are occupied by TFs, such as insulators CTCF and cohesin, that negatively regulate transcription, as well as interferon regulatory factor (IRF)5 and IRF7, that positively and distinctly regulate IFNA subtypes. A detailed understanding of the factors controlling type I IFN gene transcription will significantly aid in the identification and development of new therapeutic strategies targeting the IFN pathway in autoimmune disease.

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“…It has been described in several disorders, including autoimmune hemolytic anemia, HIV infection, type 2 diabetes, and macrovascular disease, systemic lupus erythematosus, autoimmune thrombocytopenia, aplastic anemia, and polytransfused patients with β-thalassemia major [22][23][24][25][26].…”

Section: Discussionmentioning

confidence: 99%

Altered Expression Pattern of CD55 and CD59 on Red Blood Cells in Anemia of Chronic Kidney Disease

Al-Faris

Al-Humood

Behbehani³

et al. 2017

Med Princ Pract

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Objective: The aim of this study was to investigate the expression pattern of CD55 and CD59 on red blood cells (RBCs) in anemic chronic kidney disease (CKD) patients, and factors that might influence their expression. Subjects and Methods: Nighty-oneadult anemic CKD patients and 80 healthy controls (HCs) were enrolled. Anemic CKD patients were divided into 3 subgroups based on receiving erythropoietin and renal replacement therapies. Flow cytometric analysis of CD55 and CD59 expression was performed on RBCs from blood samples obtained from CKD patients and HCs. Results: CD59 deficiency was significantly higher among CKD patients than HCs (n = 68, 74.7%, vs. n = 13, 16.3%, respectively; p < 0.001). The median proportions of CD55- and CD59-deficient RBCs in CKD patients were significantly higher compared to HCs (0.34 vs. 0.15, and 4.3 vs. 2.0, p < 0.001 and p < 0.001, respectively). The mean fluorescence intensity (MFI) of CD55 and CD59 expression was significantly lower in CKD patients compared to HCs (1.2 vs. 2.8, and 17.0 vs. 20.3, p < 0.04 and p < 0. 001, respectively). The hemoglobin level was inversely correlated with the proportions of CD55- and CD59-deficient RBCs (r = -0.37, p < 0.001, and r = -0.22, p < 0.02, respectively). The number of CD59-deficient patients was significantly different between the 3 subgroups of CKD patients (p = 0.001), and a significant difference was present in the MFI of CD55 and CD59 expression among the 3 subgroups (p = 0.04 and p = 0.03, respectively). Conclusion: The expression pattern of CD55 and CD59 on RBCs is altered in anemic CKD patients, which could play a role in the pathogenesis of anemia in CKD.

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Expression of CD55 and CD59 on peripheral blood cells from systemic lupus erythematosus (SLE) patients

Cited by 36 publications

References 26 publications

Diminished Expression of Complement Regulatory Proteins on Peripheral Blood Cells from Systemic Lupus Erythematosus Patients

Diminished Expression of Complement Regulatory Proteins on Peripheral Blood Cells from Systemic Lupus Erythematosus Patients

Bioinformatics Analysis of the Factors Controlling Type I IFN Gene Expression in Autoimmune Disease and Virus-Induced Immunity

Altered Expression Pattern of CD55 and CD59 on Red Blood Cells in Anemia of Chronic Kidney Disease

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