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[PMID]:28640379
[Au] Autor:Abdel-Latif M; Abdel-Moneim AA; El-Hefnawy MH; Khalil RG
[Ad] Endereço:Division of Immunity, Department of Zoology, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt.
[Ti] Título:Comparative and correlative assessments of cytokine, complement and antibody patterns in paediatric type 1 diabetes.
[So] Source:Clin Exp Immunol;190(1):110-121, 2017 Oct.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:One of the most widespread and effective environmental factors is the infection with enteroviruses (EVs) which accelerate ß cell destruction in type 1 diabetes (T1D). This study represented a comparison between diabetic EV and EV children as well as correlation analysis between autoantibodies, T1D markers, cytokines, complement activation products and anti-coxsackievirus (CV) immunoglobulin (Ig)G. EV RNA was detected in Egyptian children with T1D (26·2%) and healthy controls (0%). Detection of anti-CV IgG in T1D-EV resulted in 64% positivity. Within T1D-EV , previously diagnosed (PD) showed 74 versus 56% in newly diagnosed (ND) children. Comparisons between populations showed increased levels of haemoglobin A1c (HbA1c), C-reactive protein (CRP), nitric oxide (NO), glutamic acid decarboxylase and insulin and islet cell autoantibodies [glutamic acid decarboxylase autoantibodies (GADA), insulin autoantibodies (IAA) and islet cell cytoplasmic autoantibodies (ICA), respectively], interferon (IFN)-γ, tumour necrosis factor (TNF)-α, interleukin (IL)-1ß, IL -10, IL -12, IL -17, C3d and sC5-9 in T1D-EV versus T1D-EV . Conversely, both IL-20 and transforming growth factor (TGF-ß) decreased in T1D-EV versus EV , while IL-4, -6 and -13 did not show any changes. Correlation analysis showed dependency of accelerated autoimmunity and ß cell destruction on increased IFN-γ, IL-12 and IL-17 versus decreased IL-4, -6 and -13. In conclusion, IFN-γ, IL-12 and IL-17 played an essential role in exacerbating EV -T1D, while C3d, sC5b -9, IL-10 and -20 displayed distinct patterns.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Diabetes Mellitus Tipo 1/imunologia
Infecções por Enterovirus/imunologia
Enterovirus/imunologia
Ilhotas Pancreáticas/imunologia
[Mh] Termos MeSH secundário: Adolescente
Anticorpos Antivirais/metabolismo
Apoptose
Autoanticorpos/metabolismo
Criança
Pré-Escolar
Ativação do Complemento
Complemento C3d/metabolismo
Complemento C5b/metabolismo
Citocinas/genética
Diabetes Mellitus Tipo 1/complicações
Egito
Infecções por Enterovirus/complicações
Glutamato Descarboxilase/imunologia
Seres Humanos
Insulina/imunologia
Ilhotas Pancreáticas/patologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Viral); 0 (Autoantibodies); 0 (Cytokines); 0 (Insulin); 80295-45-0 (Complement C3d); 80295-55-2 (Complement C5b); EC 4.1.1.15 (Glutamate Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1111/cei.13001


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[PMID]:28610663
[Au] Autor:Nilsson PH; Thomas AM; Bergseth G; Gustavsen A; Volokhina EB; van den Heuvel LP; Barratt-Due A; Mollnes TE
[Ad] Endereço:Department of Immunology, Oslo University Hospital Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway; Linnaeus Centre for Biomaterials Chemistry, Linnaeus University, Kalmar, Sweden.
[Ti] Título:Eculizumab-C5 complexes express a C5a neoepitope in vivo: Consequences for interpretation of patient complement analyses.
[So] Source:Mol Immunol;89:111-114, 2017 Sep.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The complement system has obtained renewed clinical focus due to increasing number of patients treated with eculizumab, a monoclonal antibody inhibiting cleavage of C5 into C5a and C5b. The FDA approved indications are paroxysmal nocturnal haemoglobinuria and atypical haemolytic uremic syndrome, but many other diseases are candidates for complement inhibition. It has been postulated that eculizumab does not inhibit C5a formation in vivo, in contrast to what would be expected since it blocks C5 cleavage. We recently revealed that this finding was due to a false positive reaction in a C5a assay. In the present study, we identified expression of a neoepitope which was exposed on C5 after binding to eculizumab in vivo. By size exclusion chromatography of patient serum obtained before and after infusion of eculizumab, we document that the neoepitope was exposed in the fractions containing the eculizumab-C5 complexes, being positive in this actual C5a assay and negative in others. Furthermore, we confirmed that it was the eculizumab-C5 complexes that were detected in the C5a assay by adding an anti-IgG4 antibody as detection antibody. Competitive inhibition by anti-C5 antibodies localized the epitope to the C5a moiety of C5. Finally, acidification of C5, known to alter C5 conformation, induced a neoepitope reacting identical to the one we explored, in the C5a assays. These data are important for interpretation of complement analyses in patients treated with eculizumab.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Ativação do Complemento/efeitos dos fármacos
Complemento C5/imunologia
Complemento C5a/imunologia
Complemento C5b/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/metabolismo
Síndrome Hemolítico-Urêmica Atípica/sangue
Síndrome Hemolítico-Urêmica Atípica/tratamento farmacológico
Síndrome Hemolítico-Urêmica Atípica/imunologia
Cromatografia em Gel
Ativação do Complemento/imunologia
Complemento C5/metabolismo
Complemento C5a/metabolismo
Complemento C5b/metabolismo
Inativadores do Complemento/metabolismo
Inativadores do Complemento/uso terapêutico
Ensaio de Imunoadsorção Enzimática
Epitopos/imunologia
Epitopos/metabolismo
Hemoglobinúria Paroxística/sangue
Hemoglobinúria Paroxística/tratamento farmacológico
Hemoglobinúria Paroxística/imunologia
Seres Humanos
Concentração de Íons de Hidrogênio
Imunoglobulina G/sangue
Imunoglobulina G/imunologia
Avaliação de Resultados (Cuidados de Saúde)
Ligação Proteica/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Complement C5); 0 (Complement Inactivating Agents); 0 (Epitopes); 0 (Immunoglobulin G); 80295-54-1 (Complement C5a); 80295-55-2 (Complement C5b); A3ULP0F556 (eculizumab)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE


  3 / 99 MEDLINE  
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[PMID]:28579778
[Au] Autor:Wolf-Grosse S; Rokstad AM; Ali S; Lambris JD; Mollnes TE; Nilsen AM; Stenvik J
[Ad] Endereço:Department of Cancer Research and Molecular Medicine.
[Ti] Título:Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model.
[So] Source:Int J Nanomedicine;12:3927-3940, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Iron oxide nanoparticles (IONPs) are promising nanomaterials for biomedical applications. However, their inflammatory potential has not been fully established. Here, we used a lepirudin anti-coagulated human whole blood model to evaluate the potential of 10 nm IONPs to activate the complement system and induce cytokine production. Reactive oxygen species and cell death were also assessed. The IONPs activated complement, as measured by C3a, C5a and sC5b-9, and induced the production of pro-inflammatory cytokines in a particle-dose dependent manner, with the strongest response at 10 µg/mL IONPs. Complement inhibitors at C3 (compstatin analog Cp40) and C5 (eculizumab) levels completely inhibited complement activation and secretion of inflammatory mediators induced by the IONPs. Additionally, blockade of complement receptors C3aR and C5aR1 significantly reduced the levels of various cytokines, indicating that the particle-induced secretion of inflammatory mediators is mainly C5a and C3a mediated. The IONPs did not induce cell death or reactive oxygen species, which further suggests that complement activation alone was responsible for most of the particle-induced cytokines. These data suggest that the lepirudin anti-coagulated human whole blood model is a valuable ex vivo system to study the inflammatory potential of IONPs. We conclude that IONPs induce complement-mediated cytokine secretion in human whole blood.
[Mh] Termos MeSH primário: Ativação do Complemento
Citocinas/sangue
Compostos Férricos/química
Nanopartículas Metálicas/química
[Mh] Termos MeSH secundário: Anti-Inflamatórios/farmacologia
Anticoagulantes/farmacologia
Sobrevivência Celular
Complemento C3a/metabolismo
Complemento C5a/metabolismo
Complemento C5b/metabolismo
Inativadores do Complemento/farmacologia
Hirudinas/farmacologia
Seres Humanos
Tamanho da Partícula
Espécies Reativas de Oxigênio/sangue
Receptores de Complemento/sangue
Proteínas Recombinantes/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Anticoagulants); 0 (Complement Inactivating Agents); 0 (Cytokines); 0 (Ferric Compounds); 0 (Hirudins); 0 (Reactive Oxygen Species); 0 (Receptors, Complement); 0 (Recombinant Proteins); 1K09F3G675 (ferric oxide); 80295-42-7 (Complement C3a); 80295-54-1 (Complement C5a); 80295-55-2 (Complement C5b); Y43GF64R34 (lepirudin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S136453


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[PMID]:28060108
[Au] Autor:Rossoff JE; Schneiderman J; Chaudhury S; Arva NC
[Ad] Endereço:*Department of Pediatrics †Department of Pediatrics, Division of Hematology, Oncology and Stem Cell Transplant ‡Department of Pathology and Laboratory Medicine, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL.
[Ti] Título:Diagnostic Utility of Complement Immunohistochemical Studies in Post-Stem Cell Transplant Intestinal Thrombotic Microangiopathy: Case Report.
[So] Source:J Pediatr Hematol Oncol;39(4):282-286, 2017 May.
[Is] ISSN:1536-3678
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thrombotic complications are a significant source of morbidity and mortality following hematopoietic stem cell transplants. Among them, transplant-associated thrombotic microangiopathy (TA-TMA) is a well-recognized syndrome that can affect various organ systems. Its etiology is related to endothelial injury accompanied by complement activation. As many of the signs and symptoms of the disease are also encountered in other complications following hematopoietic stem cell transplant, it can often be difficult to establish the diagnosis based on clinical data alone. Histopathologic examination of various tissues may be performed in difficult cases. However, the microscopic features of TA-TMA also overlap with those seen in other posttransplant complications, suggesting a need for additional tests to help in diagnosis. Here we describe a patient who presented with hemolytic anemia, thrombocytopenia, renal and neurological impairment, who also developed significant bloody diarrhea. Flexible sigmoidoscopy with biopsies was performed to determine the exact etiology of his gastrointestinal bleed. A diagnosis of intestinal TA-TMA was established with the use of immunohistochemical stains for complement components C5b-9 and C4d. This is the first report that highlights the utility of complement staining on histologic sections from digestive samples to render a definitive diagnosis of intestinal TA-TMA.
[Mh] Termos MeSH primário: Enteropatias/diagnóstico
Transplante de Células-Tronco/efeitos adversos
Microangiopatias Trombóticas/diagnóstico
[Mh] Termos MeSH secundário: Criança
Complemento C4b/análise
Complemento C5b/análise
Hemorragia Gastrointestinal/etiologia
Seres Humanos
Imuno-Histoquímica
Masculino
Fragmentos de Peptídeos/análise
Microangiopatias Trombóticas/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Fragments); 80295-50-7 (Complement C4b); 80295-52-9 (complement C4d); 80295-55-2 (Complement C5b)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170107
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000000729


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[PMID]:28028157
[Au] Autor:Cohen D; Rijnink EC; Nabuurs RJ; Steup-Beekman GM; Versluis MJ; Emmer BJ; Zandbergen M; van Buchem MA; Allaart CF; Wolterbeek R; Bruijn JA; van Duinen SG; Huizinga TW; Bajema IM
[Ad] Endereço:Department of Pathology.
[Ti] Título:Brain histopathology in patients with systemic lupus erythematosus: identification of lesions associated with clinical neuropsychiatric lupus syndromes and the role of complement.
[So] Source:Rheumatology (Oxford);56(1):77-86, 2017 Jan.
[Is] ISSN:1462-0332
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Neuropsychiatric (NP) involvement is a poorly understood manifestation of SLE. We studied post-mortem histopathology in relation to clinical NPSLE syndromes and complement deposition in brains of NPSLE and SLE patients and controls. Furthermore, we investigated the correlation between cerebral post-mortem histopathology and ex vivo 7 T MRI findings in SLE and NPSLE. METHODS: A nationwide search for autopsy material yielded brain tissue from 16 NPSLE and 18 SLE patients. Brains obtained from 24 patients who died of acute cardiac events served as controls. Apart from a histopathological evaluation, paraffin-embedded cortical tissue was stained for components of the classical, lectin and terminal complement pathways. RESULTS: Diffuse vasculopathy, microinfarction, macroinfarction, vasculitis and microthrombi occurred significantly more often in NPSLE than SLE patients and were absent in controls. Focal vasculopathy was found in both SLE patients and controls. Complement deposition was strongly associated with both SLE and NPSLE, but not with controls (P < 0.001). Microthrombi were found uniquely in NPSLE and were associated with C4d and C5b-9 deposits (P < 0.05). A 7 T MRI was unable to detect most small vessel injury that was visible histopathologically. CONCLUSION: Our study demonstrates that histopathological lesions in NPSLE represent a continuum, ranging from non-specific lesions such as focal vasculopathy, to more specific lesions including C4d- and C5b-9-associated microthrombi and diffuse vasculopathy related to clinical syndromes defining NPSLE. Complement deposition may be a key factor in the interaction between circulating autoantibodies and thromboischaemic lesions observed in NPSLE. Therefore, complement inhibition may have novel therapeutic potential in NPSLE.
[Mh] Termos MeSH primário: Infarto Encefálico/patologia
Encéfalo/patologia
Trombose Intracraniana/patologia
Vasculite Associada ao Lúpus do Sistema Nervoso Central/patologia
Vasculite do Sistema Nervoso Central/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Autoanticorpos/imunologia
Autopsia
Encéfalo/diagnóstico por imagem
Encéfalo/metabolismo
Infarto Encefálico/diagnóstico por imagem
Infarto Encefálico/etiologia
Infarto Encefálico/metabolismo
Estudos de Casos e Controles
Complemento C4b/imunologia
Complemento C4b/metabolismo
Complemento C5b/imunologia
Complemento C5b/metabolismo
Complexo de Ataque à Membrana do Sistema Complemento/imunologia
Complexo de Ataque à Membrana do Sistema Complemento/metabolismo
Via Clássica do Complemento
Lectina de Ligação a Manose da Via do Complemento
Proteínas do Sistema Complemento/imunologia
Proteínas do Sistema Complemento/metabolismo
Feminino
Seres Humanos
Imuno-Histoquímica
Trombose Intracraniana/diagnóstico por imagem
Trombose Intracraniana/etiologia
Trombose Intracraniana/metabolismo
Lúpus Eritematoso Sistêmico/metabolismo
Lúpus Eritematoso Sistêmico/patologia
Vasculite Associada ao Lúpus do Sistema Nervoso Central/complicações
Vasculite Associada ao Lúpus do Sistema Nervoso Central/diagnóstico por imagem
Vasculite Associada ao Lúpus do Sistema Nervoso Central/metabolismo
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Fragmentos de Peptídeos/imunologia
Fragmentos de Peptídeos/metabolismo
Vasculite do Sistema Nervoso Central/diagnóstico por imagem
Vasculite do Sistema Nervoso Central/etiologia
Vasculite do Sistema Nervoso Central/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Complement Membrane Attack Complex); 0 (Peptide Fragments); 80295-50-7 (Complement C4b); 80295-52-9 (complement C4d); 80295-55-2 (Complement C5b); 9007-36-7 (Complement System Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE
[do] DOI:10.1093/rheumatology/kew341


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[PMID]:27027470
[Au] Autor:Wang H; Zhang JX; Ye LP; Li SL; Wang F; Zha WS; Shen T; Wu C; Zhu QX
[Ad] Endereço:a Department of Nutrition , Chaohu Hospital of Anhui Medical University , Anhui , PR China ;
[Ti] Título:Plasma Kallikrein-Kinin system mediates immune-mediated renal injury in trichloroethylene-sensitized mice.
[So] Source:J Immunotoxicol;13(4):567-79, 2016 Jul.
[Is] ISSN:1547-6901
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Trichloroethylene (TCE) is a major environmental pollutant. An immunological response is a newly-recognized mechanism for TCE-induced kidney damage. However, the role of the plasma kallikrein-kinin system (KKS) in immune-mediated kidney injury has never been examined. This study aimed to explore the role of the key components of the KKS, i.e. plasma kallikrein (PK), bradykinin (BK) and its receptors B1R and B2R, in TCE-induced kidney injury. A mouse model of skin sensitization was used to explore the mechanism of injury with or without a PK inhibitor PKSI. Kidney function was evaluated by measuring blood urea nitrogen (BUN) and creatinine (Cr) in conjunction with histopathologic characterization. Plasma BK was determined by ELISA; Renal C5b-9 membrane attack complex was evaluated by immunohistochemistry. Expression of BK and PK in the kidney was detected by immunofluorescence. mRNA and protein levels of B1R and B2R were assessed by real-time qPCR and Western blot. As expected, numerous inflammatory cell infiltration and tubular epithelial cell vacuolar degeneration were observed in TCE-sensitized mice. Moreover, serum BUN and Cr and plasma BK were increased. In addition, deposition of BK, PK and C5b-9 were observed and B1R and B2R mRNA and proteins levels were up-regulated. Pre-treatment with PKSI, a highly selective inhibitor of PK, alleviated TCE-induced renal damage. In addition, PKSI attenuated TCE-induced up-regulation of BK, PK and its receptors and C5b-9. These results provided the first evidence that activation of the KKS contributed to immune-mediated renal injury induced by TCE and also helped to identify the KKS as a potential therapeutic target for mitigating chemical sensitization-induced renal damage.
[Mh] Termos MeSH primário: Lesão Renal Aguda/imunologia
Poluição Ambiental/efeitos adversos
Sistema Calicreína-Cinina
Tricloroetileno/toxicidade
Urotélio/patologia
[Mh] Termos MeSH secundário: Animais
Nitrogênio da Ureia Sanguínea
Bradicinina/sangue
Complemento C5b/metabolismo
Creatinina/sangue
Feminino
Regulação da Expressão Gênica
Seres Humanos
Calicreínas/sangue
Camundongos
Camundongos Endogâmicos BALB C
Receptor B1 da Bradicinina/genética
Receptor B1 da Bradicinina/metabolismo
Receptor B2 da Bradicinina/genética
Receptor B2 da Bradicinina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Bradykinin B1); 0 (Receptor, Bradykinin B2); 290YE8AR51 (Trichloroethylene); 80295-55-2 (Complement C5b); AYI8EX34EU (Creatinine); EC 3.4.21.- (Kallikreins); S8TIM42R2W (Bradykinin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160331
[St] Status:MEDLINE
[do] DOI:10.3109/1547691X.2016.1142019


  7 / 99 MEDLINE  
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[PMID]:26841837
[Au] Autor:Serna M; Giles JL; Morgan BP; Bubeck D
[Ad] Endereço:Department of Life Sciences, Imperial College London, Sir Ernst Chain Building, South Kensington Campus, London SW7 2AZ, UK.
[Ti] Título:Structural basis of complement membrane attack complex formation.
[So] Source:Nat Commun;7:10587, 2016 Feb 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In response to complement activation, the membrane attack complex (MAC) assembles from fluid-phase proteins to form pores in lipid bilayers. MAC directly lyses pathogens by a 'multi-hit' mechanism; however, sublytic MAC pores on host cells activate signalling pathways. Previous studies have described the structures of individual MAC components and subcomplexes; however, the molecular details of its assembly and mechanism of action remain unresolved. Here we report the electron cryo-microscopy structure of human MAC at subnanometre resolution. Structural analyses define the stoichiometry of the complete pore and identify a network of interaction interfaces that determine its assembly mechanism. MAC adopts a 'split-washer' configuration, in contrast to the predicted closed ring observed for perforin and cholesterol-dependent cytolysins. Assembly precursors partially penetrate the lipid bilayer, resulting in an irregular ß-barrel pore. Our results demonstrate how differences in symmetric and asymmetric components of the MAC underpin a molecular basis for pore formation and suggest a mechanism of action that extends beyond membrane penetration.
[Mh] Termos MeSH primário: Complemento C5b/ultraestrutura
Complemento C6/ultraestrutura
Complemento C7/ultraestrutura
Complemento C8/ultraestrutura
Complemento C9/ultraestrutura
Complexo de Ataque à Membrana do Sistema Complemento/ultraestrutura
Complexos Multiproteicos/ultraestrutura
[Mh] Termos MeSH secundário: Cromatografia Líquida
Microscopia Crioeletrônica
Corantes Fluorescentes
Seres Humanos
Processamento de Imagem Assistida por Computador
Espectrometria de Massas
Microscopia Eletrônica
Modelos Moleculares
Estrutura Molecular
Estrutura Secundária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Complement C6); 0 (Complement C7); 0 (Complement C8); 0 (Complement C9); 0 (Complement Membrane Attack Complex); 0 (Fluorescent Dyes); 0 (Multiprotein Complexes); 80295-55-2 (Complement C5b)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160205
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms10587


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[PMID]:26335102
[Au] Autor:Thurman JM; Wong M; Renner B; Frazer-Abel A; Giclas PC; Joy MS; Jalal D; Radeva MK; Gassman J; Gipson DS; Kaskel F; Friedman A; Trachtman H
[Ad] Endereço:Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, United States of America.
[Ti] Título:Complement Activation in Patients with Focal Segmental Glomerulosclerosis.
[So] Source:PLoS One;10(9):e0136558, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Recent pre-clinical studies have shown that complement activation contributes to glomerular and tubular injury in experimental FSGS. Although complement proteins are detected in the glomeruli of some patients with FSGS, it is not known whether this is due to complement activation or whether the proteins are simply trapped in sclerotic glomeruli. We measured complement activation fragments in the plasma and urine of patients with primary FSGS to determine whether complement activation is part of the disease process. STUDY DESIGN: Plasma and urine samples from patients with biopsy-proven FSGS who participated in the FSGS Clinical Trial were analyzed. SETTING AND PARTICIPANTS: We identified 19 patients for whom samples were available from weeks 0, 26, 52 and 78. The results for these FSGS patients were compared to results in samples from 10 healthy controls, 10 patients with chronic kidney disease (CKD), 20 patients with vasculitis, and 23 patients with lupus nephritis. OUTCOMES: Longitudinal control of proteinuria and estimated glomerular filtration rate (eGFR). MEASUREMENTS: Levels of the complement fragments Ba, Bb, C4a, and sC5b-9 in plasma and urine. RESULTS: Plasma and urine Ba, C4a, sC5b-9 were significantly higher in FSGS patients at the time of diagnosis than in the control groups. Plasma Ba levels inversely correlated with the eGFR at the time of diagnosis and at the end of the study. Plasma and urine Ba levels at the end of the study positively correlated with the level of proteinuria, the primary outcome of the study. LIMITATIONS: Limited number of patients with samples from all time-points. CONCLUSIONS: The complement system is activated in patients with primary FSGS, and elevated levels of plasma Ba correlate with more severe disease. Measurement of complement fragments may identify a subset of patients in whom the complement system is activated. Further investigations are needed to confirm our findings and to determine the prognostic significance of complement activation in patients with FSGS.
[Mh] Termos MeSH primário: Ativação do Complemento
Glomerulosclerose Segmentar e Focal/sangue
Glomerulosclerose Segmentar e Focal/urina
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Complemento C5b/metabolismo
Complemento C5b/urina
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
80295-55-2 (Complement C5b)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150904
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0136558


  9 / 99 MEDLINE  
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[PMID]:25795308
[Au] Autor:Blom AM; Österborg A; Mollnes TE; Okroj M
[Ad] Endereço:Department of Laboratory Medicine Malmö, Section of Medical Protein Chemistry, Lund University, Inga Marie Nilssons Street 53, 20502 Malmö, Sweden.
[Ti] Título:Antibodies reactive to cleaved sites in complement proteins enable highly specific measurement of soluble markers of complement activation.
[So] Source:Mol Immunol;66(2):164-70, 2015 Aug.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:An emerging number of diseases and therapeutic approaches with defined involvement of the complement system justify a need for specific markers reflecting activation of particular effector arms of the complement cascade. Measurement of such soluble markers in circulation is a challenge since the specificity of antibodies must be limited to activated complement fragments but not predominant and ubiquitous parental molecules. Existing assays for the measurement of soluble, activated complement proteins are based on the detection of conformational neoepitopes. We tested an alternative approach based on detection of short linear neoepitopes exposed at the cleavage sites after activation of the actual complement component. Obtained antibodies reactive to C4d and C5b fragments enabled us to set up highly specific sandwich ELISAs, which ensured trustful measurements without false positive readouts characteristic for some of the widely used assays.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica
Complemento C5b/metabolismo
Ensaio de Imunoadsorção Enzimática/métodos
Neoplasias Hematológicas/sangue
Fragmentos de Peptídeos/sangue
[Mh] Termos MeSH secundário: Animais
Anticorpos/química
Anticorpos/isolamento & purificação
Ativação do Complemento
Complemento C4b/química
Complemento C4b/imunologia
Complemento C5b/química
Complemento C5b/imunologia
Neoplasias Hematológicas/tratamento farmacológico
Neoplasias Hematológicas/imunologia
Neoplasias Hematológicas/patologia
Seres Humanos
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/imunologia
Proteólise
Coelhos
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies); 0 (Peptide Fragments); 80295-50-7 (Complement C4b); 80295-52-9 (complement C4d); 80295-55-2 (Complement C5b)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:150608
[Lr] Data última revisão:
150608
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150322
[St] Status:MEDLINE


  10 / 99 MEDLINE  
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[PMID]:25735751
[Au] Autor:Shi H; Williams JA; Guo L; Stampoulis D; Francesca Cordeiro M; Moss SE
[Ad] Endereço:Department of Cell Biology, UCL Institute of Ophthalmology, 11-43 Bath Street, London, EC1V 9EL, UK.
[Ti] Título:Exposure to the complement C5b-9 complex sensitizes 661W photoreceptor cells to both apoptosis and necroptosis.
[So] Source:Apoptosis;20(4):433-43, 2015 Apr.
[Is] ISSN:1573-675X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The loss of photoreceptors is the defining characteristic of many retinal degenerative diseases, but the mechanisms that regulate photoreceptor cell death are not fully understood. Here we have used the 661W cone photoreceptor cell line to ask whether exposure to the terminal complement complex C5b-9 induces cell death and/or modulates the sensitivity of these cells to other cellular stressors. 661W cone photoreceptors were exposed to complete normal human serum following antibody blockade of CD59. Apoptosis induction was assessed morphologically, by flow cytometry, and on western blotting by probing for cleaved PARP and activated caspase-3. Necroptosis was assessed by flow cytometry and Sirtuin 2 inhibition using 2-cyano-3-[5-(2,5-dichlorophenyl)-2-furyl]-N-5-quinolinylacrylamide (AGK2). The sensitivity of 661W cells to ionomycin, staurosporine, peroxide and chelerythrine was also investigated, with or without prior formation of C5b-9. 661W cells underwent apoptotic cell death following exposure to C5b-9, as judged by poly(ADP-ribose) polymerase 1 cleavage and activation of caspase-3. We also observed apoptotic cell death in response to staurosporine, but 661W cells were resistant to both ionomycin and peroxide. Interestingly, C5b-9 significantly increased 661W sensitivity to staurosporine-induced apoptosis and necroptosis. These studies show that low levels of C5b-9 on 661W cells can induce apoptosis, and that C5b-9 specifically sensitizes 661W cells to certain apoptotic and necroptotic pathways. Our observations provide new insight into the potential role of the complement system in photoreceptor loss, with implications for the molecular aetiology of retinal disease.
[Mh] Termos MeSH primário: Apoptose
Complemento C5b/metabolismo
Complemento C6/metabolismo
Complemento C7/metabolismo
Complemento C8/metabolismo
Complemento C9/metabolismo
Células Fotorreceptoras/citologia
Células Fotorreceptoras/metabolismo
[Mh] Termos MeSH secundário: Caspase 3/metabolismo
Linhagem Celular
Complexo de Ataque à Membrana do Sistema Complemento/metabolismo
Seres Humanos
Necrose
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Complement C6); 0 (Complement C7); 0 (Complement C8); 0 (Complement C9); 0 (Complement Membrane Attack Complex); 0 (SC5b-9 protein complex); 80295-55-2 (Complement C5b); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150305
[St] Status:MEDLINE
[do] DOI:10.1007/s10495-015-1091-7



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