published_or_final_version / Medicine / Doctoral / Doctor of Philosophy

Objective: to assess the prevalence of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and spondyloarthropathy (SpA) in Vilnius, Lithuania. Methods: 3 prevalence studies were conducted: 1. Registry-based study of the prevalence of RA and SLE; 2. Population-based study of the prevalence of RA and SLE (interview conducted by mail); 3. Poulation-based study of the prevalence of RA and SpA (interview conducted by telephone). Results: according to the Vilnius RA and SLE registry, the prevalence of RA in Vilnius at the end of year 2004 was 0,14% (95% CI 0,13-0,15), and the prevalence of SLE was 0,0174% or 17,4/100 000 (95% CI 0,0137-0,0218). The population-based study, conducted by mail, revealed 15 RA and 2 SLE cases, accounting for a prevalence rate of RA of 0,37% (95% CI 0,21-0,62), and a prevalence of SLE rate of 0,0498% (95% CI 0,006-0,180). The standardized prevalence rate according to age and sex in the Vilnius population showed an RA prevalence of 0,32% (95% CI 0,18-0,57). The population-based study, conducted be telephone, detected 16 RA and 13 SpA cases, resulting in a crude prevalence of 0,76% (95% CI 0,44-1,24) for RA and 0,62% (95% CI 0,33-1,06) for SpA. The standardized prevalence rate according to age and sex in the Vilnius population showed an RA prevalence of 0,51% (95% CI 0,29-0,96) and a SpA prevalence of – 0,75% (95% CI 0,38-1,40). / Darbo tikslas: nustatyti reumatoidinio artrito (RA), seronegatyvių spondiloartropatijų (SpA) bei sisteminės raudonosios vilkligės (SRV) paplitimą Vilniaus mieste. Darbo metodika: Buvo atlikti 3 tyrimai: 1. RA ir SRV paplitimo Vilniaus mieste apskaičiavimas, remiantis Vilniaus miesto RA ir SRV sergančių asmenų duomenų baze; 2. RA ir SRV paplitimo Vilniaus mieste populiacinis tyrimas, apklausiant Vilniaus miesto gyventojus paštu; 3. RA ir SpA paplitimo Vilniaus mieste populiacinis tyrimas, apklausiant Vilniaus miesto gyventojus telefonu. Rezultatai: remiantis Vilniaus miesto RA ir SRV sergančiųjų duomenų baze, RA paplitimas Vilniaus mieste 2004m. pabaigoje buvo 0,14% (95% PI 0,13-0,15). Apskaičiuotas SRV paplitimas Vilniuje 2004m. pabaigoje buvo 0,0174% arba 17,4/100 000 gyventojų (95% PI 0,0137-0,0218). Atlikus RA ir SRV paplitimo tyrimą (apklausą paštu), nustatyta, kad RA paplitimas Vilniuje yra 0,37% (95% PI 0,21-0,62), o SRV paplitimas – 0,0498% (95% PI 0,006-0,180). RA paplitimas buvo standartizuotas pagal amžių ir lytį, remiantis 2004m. pradžios Vilniaus miesto populiacija, apskaičiuotas standartizuotas RA paplitimas yra 0,32% (95% PI 0,18-0,57). Atlikus RA ir SpA paplitimo tyrimą (apklausą telefonu), apskaičiuotas RA paplitimas buvo 0,76% (95% PI 0,44-1,24), o SpA paplitimas - 0,62% (95% PI 0,33-1,06). RA ir SpA paplitimas buvo standartizuotas pagal amžių ir lytį, remiantis 2004m. pradžios Lietuvos populiacija, apskaičiuotas standartizuotas RA paplitimas yra 0,51% (95%... [toliau žr. visą tekstą]

Darbo tikslas: nustatyti reumatoidinio artrito (RA), seronegatyvių spondiloartropatijų (SpA) bei sisteminės raudonosios vilkligės (SRV) paplitimą Vilniaus mieste. Darbo metodika: Buvo atlikti 3 tyrimai: 1. RA ir SRV paplitimo Vilniaus mieste apskaičiavimas, remiantis Vilniaus miesto RA ir SRV sergančių asmenų duomenų baze; 2. RA ir SRV paplitimo Vilniaus mieste populiacinis tyrimas, apklausiant Vilniaus miesto gyventojus paštu; 3. RA ir SpA paplitimo Vilniaus mieste populiacinis tyrimas, apklausiant Vilniaus miesto gyventojus telefonu. Rezultatai: remiantis Vilniaus miesto RA ir SRV sergančiųjų duomenų baze, RA paplitimas Vilniaus mieste 2004m. pabaigoje buvo 0,14% (95% PI 0,13-0,15). Apskaičiuotas SRV paplitimas Vilniuje 2004m. pabaigoje buvo 0,0174% arba 17,4/100 000 gyventojų (95% PI 0,0137-0,0218). Atlikus RA ir SRV paplitimo tyrimą (apklausą paštu), nustatyta, kad RA paplitimas Vilniuje yra 0,37% (95% PI 0,21-0,62), o SRV paplitimas – 0,0498% (95% PI 0,006-0,180). RA paplitimas buvo standartizuotas pagal amžių ir lytį, remiantis 2004m. pradžios Vilniaus miesto populiacija, apskaičiuotas standartizuotas RA paplitimas yra 0,32% (95% PI 0,18-0,57). Atlikus RA ir SpA paplitimo tyrimą (apklausą telefonu), apskaičiuotas RA paplitimas buvo 0,76% (95% PI 0,44-1,24), o SpA paplitimas - 0,62% (95% PI 0,33-1,06). RA ir SpA paplitimas buvo standartizuotas pagal amžių ir lytį, remiantis 2004m. pradžios Lietuvos populiacija, apskaičiuotas standartizuotas RA paplitimas yra 0,51% (95%... [toliau žr. visą tekstą] / Objective: to assess the prevalence of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and spondyloarthropathy (SpA) in Vilnius, Lithuania. Methods: 3 prevalence studies were conducted: 1. Registry-based study of the prevalence of RA and SLE; 2. Population-based study of the prevalence of RA and SLE (interview conducted by mail); 3. Poulation-based study of the prevalence of RA and SpA (interview conducted by telephone). Results: according to the Vilnius RA and SLE registry, the prevalence of RA in Vilnius at the end of year 2004 was 0,14% (95% CI 0,13-0,15), and the prevalence of SLE was 0,0174% or 17,4/100 000 (95% CI 0,0137-0,0218). The population-based study, conducted by mail, revealed 15 RA and 2 SLE cases, accounting for a prevalence rate of RA of 0,37% (95% CI 0,21-0,62), and a prevalence of SLE rate of 0,0498% (95% CI 0,006-0,180). The standardized prevalence rate according to age and sex in the Vilnius population showed an RA prevalence of 0,32% (95% CI 0,18-0,57). The population-based study, conducted be telephone, detected 16 RA and 13 SpA cases, resulting in a crude prevalence of 0,76% (95% CI 0,44-1,24) for RA and 0,62% (95% CI 0,33-1,06) for SpA. The standardized prevalence rate according to age and sex in the Vilnius population showed an RA prevalence of 0,51% (95% CI 0,29-0,96) and a SpA prevalence of – 0,75% (95% CI 0,38-1,40).

Autoimmune diseases are clinical manifestations of a loss-of-tolerance of the immune system against the body’s own substances and healthy tissues. Primary Sjögren’s syndrome (pSS) and systemic lupus erythematosus (SLE) are two chronic inflammatory autoimmune diseases characterized by autoantibody production and an activated type I interferon system. Although the precise mechanisms leading to autoimmune processes are not well defined, recent studies suggest that aberrant DNA methylation and gene expression patterns may play a central role in the pathogenesis of these disorders. The aim of this thesis was to investigate DNA methylation and gene expression in pSS and SLE on a genome-wide scale to advance our understanding of how these factors contribute to the diseases and to identify potential biomarkers and novel treatment targets. In study I, differential DNA methylation was analyzed in multiple tissues from pSS patients and healthy controls. We identified thousands of CpG sites with perturbed methylation; the most prominent finding was a profound hypomethylation at regulatory regions of type I interferon induced genes in pSS. In study II, a cases-case study comparing DNA methylation in pSS patients with high fatigue to patients with low fatigue, we found methylation patterns associated to the degree of fatigue. In study III, RNA-sequencing was applied to investigate the transcriptome of B cells in pSS in comparison to controls. Increased expression of type I and type II interferon regulated genes in pSS was observed, indicating ongoing immune activation in B cells. In study IV, the impact of DNA methylation on disease susceptibility and phenotypic variability in SLE was investigated. We identified DNA methylation patterns associated to disease susceptibility, SLE manifestations and different treatments. In addition, we mapped methylation quantitative trait loci and observed evidence for genetic regulation of DNA methylation in SLE.   In conclusion, the results presented in this thesis provide new insights into the molecular mechanisms underlying autoimmunity in pSS and SLE. The studies confirm the central role of the interferon system in pSS and SLE and further suggest novel genes and mechanisms to be involved in the pathogenesis these autoimmune diseases.

Two novel B cell populations were characterized in peripheral blood of patients with common variable immunodeficiency and healthy controls were observed using flow cytometry in the study supported by the grant IGA MZ ČR NKT11414-3. These B cell populations were defined as CD19+ CD27- CD21+ CD38low CD24+ IgM+ FO I and CD19+ CD27- CD21+ CD38low CD24++ IgM++ cells. Since none of found populations has ever been described, the aim of this thesis was to characterize these populations with focus on analysis of variable regions of the heavy chains of immunoglobulins and genes coding proteins participating in the process of VHDHJH formation (Rag 1, Rag 2, and TdT) produced by cells of these populations. Flow cytometry, single cell sorting, single-cell RT-PCR, IgVH, Rag 1, Rag 2, and TdT specific PCR amplification and cycle sequencing were employed to perform the molecular analysis in individual B lymphocytes. Both populations in two patients with common variable immunodeficiency, two healthy controls, and in two patients with autoimmune diseases - rheumatoid arthritis and systemic lupus erythematosus (as the disease control) - were examined. Finally, the statistical analysis was used to evaluate the differences in expression of variable regions of the heavy chains of immunoglobulins and in Rag1 and 2, and...

Introdução: Os anticorpos antiproteína P ribossomal (anti-P) são considerados marcadores sorológicos específicos do Lúpus Eritematoso Sistêmico (LES) e estão associados a acometimento hepático nesta doença. As semelhanças entre a hepatite autoimune (HAI) e a hepatite associada ao LES levou ao questionamento se o anticorpo anti-P também estaria presente na HAI. Objetivo: Avaliar a frequência e significância clínica do anticorpo anti-P em uma grande coorte de pacientes com HAI. Métodos: Foram analisados os soros de 96 pacientes com HAI, coletados no diagnóstico e comparados com 82 soros de indivíduos saudáveis. Todos os soros foram testados para a presença do anticorpo anti-P pelo método de ELISA, do anticorpo anti-DNA de dupla fita pelo método de imunofluorescência indireta usando Crithidia luciliae e do anticorpo anti-Sm pelo método de ELISA. Os critérios de exclusão adotados foram a presença de outros anticorpos específicos de LES como o anti-DNA de dupla fita (n=1) e o anti-Sm (n=2) ou se o paciente apresentasse o diagnóstico de LES definido pelo Colégio Americano de Reumatologia (n=0). Os prontuários médicos foram revisados para dados demográficos, clínicos e resultados de exames laboratoriais relacionados a hepatopatia e anticorpos específicos de HAI. Resultado: Títulos moderados ou alto (> 40 U) de anti-P foram encontrados em 9,7% (9/93) dos pacientes com HAI e em nenhum dos controles (p = 0,003). No diagnóstico, os pacientes com anti-P positivo ou negativo apresentavam características demográficas/clínicas semelhantes, como a frequência de cirrose (44,4% vs 28,5%, p = 0,44) e exames laboratoriais relacionados a hepatite (p > 0,05). Entretanto, ao final do seguimento destes pacientes (média de 10,2 ± 4,9 anos), os pacientes positivos para anticorpos anti-P apresentaram uma maior frequência de cirrose quando comparados a pacientes negativos para anti-P (100% vs 60%, p = 0,04). Conclusão: a demonstração da presença do anticorpo anti-P em pacientes com HAI sem evidência de LES sugere um mecanismo comum de acometimento hepático nestas duas doenças. Além disso, a presença deste anticorpo parece predizer um pior prognóstico nos pacientes com HAI / Background: Autoantibodies to ribosomal P proteins (anti-rib P) are specific serological markers for systemic lupus erythematosus (SLE) and are associated with liver involvement in this disease. The similarity in autoimmune background between autoimmune hepatitis (AIH) and SLE- associated hepatitis raises the possibility that anti-rib P antibodies might also have relevance in AIH. Aims: To evaluate the frequency and clinical significance of anti-rib P antibodies in a large AIH cohort. Methods: Sera obtained at diagnosis of 96 AIH patients and of 82 healthy controls were tested for IgG anti-ribosomal P protein by ELISA. All of the sera were also screened for other lupus-specific autoantibodies, three patients with the presence of anti-dsDNA (n=1) and anti-Sm (n = 2) were excluded. Results: Moderate to high titers (> 40 U) of anti-rib P antibody were found in 9.7% (9/93) of the AIH patients and none of the controls (P = 0.003). At presentation, AIH patients with and without anti-rib P antibodies had similar demographic/clinical features, including the frequency of cirrhosis (44.4% vs. 28.5%, P = 0.44), hepatic laboratorial findings (p > 0.05). Importantly, at the final observation (follow-up period 10.2 ± 4.9 years), the AIH patients with anti-rib P had a significantly higher frequency of cirrhosis compared to the negative group (100% vs. 60%, P = 0.04). Conclusion: The novel demonstration of anti-rib P in AIH patients without clinical or laboratory evidence of SLE suggests a common underlying mechanism targeting the liver in these two diseases. In addition, this antibody appears to predict the patients with worse AIH prognoses

Proteinúria é a principal manifestação da nefrite lúpica (NL) e reflete lesão no podócito. Análise dos biomarcadores do podócito foi realizada com o objetivo de identificar se o fenótipo podocitário é distinto na NL membranosa pura e proliferativa. Expressão de sinaptopodina, proteína 1 do tumor de Wilms (Wilms tumor protein 1 - WT1), proteína epitelial glomerular 1 (glomerular epitelial protein 1 - GLEPP1) e nefrina foi avaliada em 52 biópsias de NL por imunohistoquímica. Expressão preservada de sinaptopodina foi observada em apenas 10 (19,2%) de todas as biópsias enquanto que 42 (80,8%) apresentavam expressão reduzida. Ambos os grupos tinham proteinúria semelhante no momento da biópsia (p = 0,22), porém, no seguimento médio de quatro anos houve uma tendência para menores níveis médios de proteinúria nos pacientes com marcação preservada de sinaptopodina (0,26 ± 0,23 vs 0,84 ± 0,90 g/24 h, p = 0,05) do que naqueles com expressão reduzida. Trinta e nove (75%) biópsias foram classificadas como proliferativa e treze (25%) como membranosa pura. Comparação dos biomarcadores do podócito demonstrou predomíno de marcação preservada de sinaptopodina (69,2%), WT1 (69,2%), GLEPP1 (53,9%) e nefrina (60%) no grupo membranosa pura enquanto apenas < 10% das proliferativas apresentaram expressão preservada. Nossos dados sugerem que nas classes proliferativas parece haver lesão estrutural do podócito, enquanto que na membranosa pura o padrão predominantemente preservado sugere uma lesão funcional do podócito que pode ser responsável pelo melhor prognóstico a longo prazo do desfecho da proteinúria / Proteinuria is a major feature of lupus nephritis (LN) and reflects podocyte injury. Analysis of podocyte biomarkers was performed attempting to identify if podocyte phenotype is distinct in pure membranous and proliferative LN. Expression of synaptopodin, Wilms tumor protein 1 (WT1), glomerular epithelial protein 1 (GLEPP1) and nephrin was evaluated in 52 LN biopsies by immunohistochemistry. Preserved synaptopodin expression was observed in only 10 (19,2%) of all biopsies while 42 (80,8%) had a reduced expression. Both groups had comparable proteinuria at the time of biopsy (p=0,22), however, in the mean follow-up of four years there was a tendency to lower mean levels of proteinuria in patients with preserved synaptopodin staining (0,26 ± 0,23 vs. 0,84 ± 0,90 g/24 h, p=0,05) than those with diminished expression. Thirty-nine (75%) biopsies were classified as proliferative and thirteen (25%) as pure membranous. Comparison of podocyte biomarkers demonstrated a predominance of preserved staining of synaptopodin (69,2%), WT1 (69,2%), GLEPP1 (53,9%) and nephrin (60%) in the pure membranous group whereas only < 10% of the proliferative showed preserved expression. Our data suggest that in proliferative forms there seems to occur structural podocyte damage, whereas in the pure membranous the predominant preserved pattern suggests a dysfunctional podocyte lesion that may account for the better long-term prognosis of proteinuria outcome

The purpose of this study was 1) to examine the significance of a patient’s active or passive role in terms of his/her health management; 2) to determine if a relationship exists between one’s active and passive scores and his/her self-directed learning readiness, and 3) to identify if his/her view of one’s self as a patient (when diagnosed with a chronic disease) impacted his/her own personal health management. Utilizing the quantitative analysis of The Self-Directed Learning Readiness Scale and the Vanderbilt Pain Management Inventory, 81 individuals’ descriptive statistics were analyzed. Self-directed learning was found to positively influence an individual’s ability to be an active patient. The moderated demographic characteristics of age, ethnicity, education level, and gender did not have a direct relationship between selfdirected learning readiness and active/passive coping groups. Further, it was established that the majority of the participants within the study, 83.75%, considered themselves an active patient managing their lupus diagnosis. However, 16.25% of the participants did not believe that they were actively managing their illness. Self-directed learning characteristics were examined through the responses to an open-ended question. The two most prevalent themes pertained to active coping and control. Characteristics of self-directed learning readiness appeared predominant amongst the responses, particularly goal-orientation and accepting responsibility for learning. Minimal themes regarding planning and enjoying learning were provided within the data. These characteristics were identified throughout the study in hopes of further research and program implementations that will help to develop leadership abilities and activity levels of self-health management in chronically ill patients. This will enable lupus patients to have a more positive outcome, it will help them successfully manage their own health, and it will improve their overall quality of life. / Includes bibliography. / Dissertation (Ph.D.)--Florida Atlantic University, 2016. / FAU Electronic Theses and Dissertations Collection

This study evaluated two methods for the isolation and purification of anti-DNA antibodies. A two-step affinity purification with streptavidin (SA) biotinylated oligodeoxythymidine (dT) M-280 and protein G Dynabeadsª was compared to a two step method using Melon(TM) Gel and cellulose DNA. Although Melon gel allowed for faster antibody purification and a higher recovery rate it gave a product of less purity than the magnetic bead method. Further characterization of the antibodies was done by PhastGel(TM) non-reducing SDS-PAGE and isoelectric focusing in order to analyze purity and confirm the polyclonal nature of anti-DNA antibodies. Agilent 2100, with a higher resolution then SDS-PAGE, revealed possible subclasses of different MW not detected by SDS-PAGE. ELISA showed that all four IgG antibody subclasses were present, while Western blot confirmed the presence of human IgGs. Ultraviolet spectroscopy, Agilent, and fluorescence based assays were used to demonstrate DNA hydrolytic activity of purified anti-DNA antibody. / by Anna M. Kats. / Thesis (M.S.)--Florida Atlantic University, 2008. / Includes bibliography. / Electronic reproduction. Boca Raton, FL : 2008 Mode of access: World Wide Web.

O lúpus eritematoso sistêmico (LES) é uma doença autoimune e protótipo das doenças por imunocomplexos (IC). A deposição de IC em tecidos ou órgãos leva a um processo inflamatório crônico, que resulta em lesão tecidual. A fisiopatologia deste processo envolve principalmente o sistema do complemento (SC), receptores de IgG (Fc?R), neutrófilos e moléculas de adesão. Os produtos de ativação SC atraem os neutrófilos para o foco inflamatório e sua interação com os IC depositados resulta na liberação de espécies reativas de oxigênio (ERO) e das enzimas dos neutrófilos sobre os tecidos. As ERO podem levar a danos nas estruturas celulares devido ao estresse oxidativo, resultando na exposição de autoantígenos e sustentação da autoimunidade. Várias anormalidades envolvendo neutrófilos, função e expressão dos Fc?R e CR foram descritas no LES. O objetivo deste estudo foi avaliar se essas alterações podem ter implicações para o dano tecidual através do depósito de IC. Devido à importância das interações neutrófilo-endotélio-SC para a inflamação e lesão tecidual por IC no LES, este estudo propôs avaliar o efeito da ativação de neutrófilos e produtos do SC sobre as células endoteliais in vitro. Os resultados mostram que a exposição das células endoteliais aos neutrófilos/LES ativo, sem estímulo, resulta em maior peroxidação lipídica comparada com o controle espontâneo, o que não foi observado com neutrófilos/saudáveis. Contudo, na presença de IC/SHN, a peroxidação lipídica foi maior quando as células endoteliais foram expostas aos neutrófilos/LES inativo comparada ao controle espontâneo. O efeito da ativação dos neutrófilos, em todos os grupos, sobre a peroxidação lipídica das células endoteliais foi dependente da opsonização dos IC pelo complemento (IC/SHN), uma vez que não foi observado quando as proteínas do complemento foram inativadas (IC/SHI). Não houve diferença na produção de ERO entre os neutrófilos dos grupos estudados. Observou-se menor expressão dos Fc?RIIa (CD32) e CR1 em neutrófilos/LES ativo, quando comparados com o grupo controle. Houve maior liberação de catalase pelos neutrófilos/LES, quando estes foram estimulados via Fc?R, e maior produção de glutationa por neutrófilos/LES inativo quando estas células foram estimuladas via Fc?R e CR. A expressão de ICAM-1 não foi diferente entre os grupos de neutrófilos, entretanto foi menor na ausência de complemento. Não houve diferença na medida da ativação da via clássica do complemento avaliada pelo fragmento C4d. Estes resultados mostram que as células endoteliais são mais suscetíveis à peroxidação lipídica na presença de neutrófilos/LES. Contudo, quando o complemento do soro é inativado, esta suscetibilidade desaparece, bem como há menor liberação de ICAM-1 por todos os grupos de neutrófilos e maior liberação de catalase por neutrófilos/LES. A interação dos neutrófilos/LES com células endoteliais pode ser deletéria para este último e depender da atividade das proteínas do sistema complemento. O modelo desenvolvido neste estudo pode contribuir para a compreensão do envolvimento dos neutrófilos e do SC nas lesões teciduais no LES. / Systemic lupus erythematosus (SLE) is an autoimmune disease and prototype of immune complex diseases (IC). The deposition of IC in tissues or organs leads to a chronic inflammatory process, which results in tissue injury. The pathophysiology of this process mainly involves the complement system (SC), IgG (Fc?R) receptors, neutrophils and adhesion molecules. SC activation products attract neutrophils to the inflammatory focus and their interaction with deposited IC results in the release of reactive oxygen species (ROS) and neutrophil enzymes into tissues. ROS can lead to damage to cell structures due to oxidative stress, resulting in the exposure of autoantigens and the support of autoimmunity. Several abnormalities involving neutrophils, function and expression of Fc?R and CR have been described in SLE. The aim of this study was to assess whether these changes may have implications for tissue damage through the deposition of IC. Due to the importance of neutrophil-endothelial-SC interactions for inflammation and tissue damage by IC in SLE, this study proposed to evaluate the effect of the activation of neutrophils and SC products on endothelial cells in vitro. The results show that exposure of endothelial cells to active neutrophils / SLE without stimulus results in higher lipid peroxidation compared to spontaneous control, which was not observed with neutrophils / healthy. However, in the presence of IC / complement from normal human serum (NHS), lipid peroxidation was greater when endothelial cells were exposed to inactive neutrophils / SLE compared to spontaneous control. The effect of neutrophil activation in all groups on endothelial cell lipid peroxidation was dependent on IC with complement (IC / NHS), as it was not observed when complement proteins were inactivated (IC / INHS). There was no difference in ROS production among the neutrophils of the studied groups. Lower expression of Fc?RIIa (CD32) and CR1 in active neutrophils / SLE, when compared with the control group, was observed. There was greater release of catalase by neutrophils / SLE, when they were stimulated via Fc?R, and increased production of glutathione by neutrophils / inactive SLE when these cells were stimulated via Fc?R and CR. There was no difference in expression of ICAM-1 between the neutrophil groups, however it was lower in the absence of complement. There was no difference in the extent of the activation of the classical complement pathway evaluated by the C4d fragment. These results show that endothelial cells are more susceptible to lipid peroxidation in the presence of neutrophils / SLE. However, when serum complement is inactivated, this susceptibility disappears, as well as there is a lower release of ICAM-1 by all neutrophil groups and greater release of catalase by neutrophils / SLE. The interaction of neutrophils / SLE with endothelial cells may be deleterious to the latter and depends on the activity of the complement system proteins. The model developed in this study may contribute to the understanding of neutrophil and SC involvement in tissue lesions in SLE.