Role of nuclear antigens and antinuclear antibodies in inflammation

1968 ◽  
Vol 17 ◽  
pp. 77-86 ◽  
Author(s):  
Eugene V. Barnett
2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
T M Matajira Chia ◽  
M Castineira Busto ◽  
M Cespon Fernandez ◽  
B Gimena Reyes ◽  
F Calvo Iglesias ◽  
...  

Abstract A 61-year-old man was admitted to the hospital with an atypical pain lumbar with oligoanuria. Other comorbidities were: arterial hypertension, diabetes mellitus and smoking .On examination the patient was comfortable at rest, with a heart rate of 89 b.p.m. and a blood pressure of 147/2 mmHg. Normal S1 and S2 heart sounds were present. There were no signs of heart failure present. Patients complained of pain in hypogastrium on palpation. Creatinine 2.33 mg / dL. PCR 72. The immunological studies were normal (including IgG and IgA serological levels, antinuclear antibodies, extractable nuclear antigens, anti-neutrophil cytoplasmic antibodies. An Body CT was performed, it shows mass that includes the ureters as well as the iliac arteries and parietal thickening in aorta wall. The positron emission tomography–computed tomography (PET CT) scans was performed that evidences pathological hypermetabolism that surrounds both primitive iliac arteries with maximum SUV 12 g / ml. Pathological hypermetabolism in ascending aorta until reaching arch with maximum SUV of 9.1 mg / ml compatible with periaortitis in the ascending aorta. A study was completed with retroperitoneal mass biopsy that showed areas of retroperitoneal fibrosis with predominantly lymphoplasmacytic areas. IgG4 / IgG> 40% , Obliterative involvement of small venules suggestive of IgG4 disease. A transthoracic echocardiogram was performed which showed normal biventricular function, absence of significant valvular disease and thickening of the aortic wall compatible with periaortitis. The patient started glucocorticoid therapy with favorable response. A PET CT control was performed that showed disappearing retroperitoneal masses around iliac vessels and disappearance of activity in lateral wall of aorta and decrease activity about ascendent aorta. DIAGNOSIS : IgG4 -related aortitis Abstract P273 Figure.


2021 ◽  
Vol 19 (1) ◽  
pp. 237-244
Author(s):  
Youssef EL Hassouni ◽  
Mohammed Bourhia ◽  
Ahmed Bari ◽  
Riaz Ullah ◽  
Hafiz Majid Mahmood ◽  
...  

Abstract Autoimmune diseases are pathological conditions in which the immune system mistakenly attacks its own tissues. This study evaluates the performance of two techniques, which are identifiers of autoantibody specifics: immunoblot and immunodot. This study was conducted in 300 patients of whom 62 were tested positive for antinuclear antibodies. The patients were initially screened for antinuclear antibodies using indirect immunofluorescence. Then, the identification of specific autoantibodies such as anti-extractable nuclear antigens (ENAs) was carried out using the immunoblot and immunodot techniques. The results showed that immunoblot and immunodot did not present a significant difference in their sensitivity against anti-SSA/52, SSB, CENP-B, PCNA, U1-snRNP, Jo-1, Pm-scl, and Mi-2 (p > 0.05). However, the two techniques showed a significant difference in their sensitivity toward autoantibodies anti-DNAn, anti-histone, anti-SmD1, and anti-ds-DNA (p < 0.05). The immunoblot data were in complete accordance with the immunodot data (100%) regarding the detection of autoantibodies such as anti SSA/52, SSB, CENP-B, PCNA, U1-snRP, Jo-1, Pm-scl, and Mi-2, 80% regarding SmD1, and 75% concerning ds-DNA. We should certainly pay closer attention to the efficiency of the techniques used in the diagnosis of autoimmune diseases.


Antibodies ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 69
Author(s):  
Yasmine Lamri ◽  
Nicolas Charles

Systemic lupus erythematosus (SLE) is a multifactorial chronic autoimmune disease, marked by the presence of autoantibodies to nuclear antigens belonging to different isotype classes. For several years, IgE antibodies have been incriminated in the development of allergic diseases and parasitic infections and different anti-IgE therapies have been developed to encounter the pathogenic role of IgE in these pathologies. Recently, multiple studies showed the presence of elevated total IgE levels and demonstrated a pathogenic role of autoreactive IgE in SLE. This review aims to summarize the findings incriminating IgE and autoreactive IgE in the pathophysiology of SLE, to describe their functional outcomes on their targeted cells as well as to discuss different IgE-related therapeutic modalities that emerged and that may be beneficial for SLE patient care.


2020 ◽  
Vol 48 (1) ◽  
pp. 18-25
Author(s):  
José Enrique Oliva Menacho ◽  
Jorge Luis Arroyo-Acevedo ◽  
José Arturo Oliva-Candela ◽  
Marco Antonio García-Hjarles ◽  
Lester Domínguez-Huarcaya

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Manfred Relle ◽  
Andreas Schwarting

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of autoantibodies against nuclear antigens and a systemic inflammation that can damage a broad spectrum of organs. SLE patients suffer from a wide variety of symptoms, which can affect virtually almost any tissue. As lupus is difficult to diagnose, the worldwide prevalence of SLE can only be roughly estimated to range from 10 and 200 cases per 100,000 individuals with dramatic differences depending on gender, ethnicity, and location. Although the treatment of this disease has been significantly ameliorated by new therapies, improved conventional drug therapy options, and a trained expert eye, the underlying pathogenesis of lupus still remain widely unknown. The complex etiology reflects the complex genetic background of the disease, which is also not well understood yet. However, in the past few years advances in lupus genetics have been made, notably with the publication of genome-wide association studies (GWAS) in humans and the identification of susceptibility genes and loci in mice. This paper reviews the role of MHC-linked susceptibility genes in the pathogenesis of systemic lupus erythematosus.


2014 ◽  
Vol 41 (7) ◽  
pp. 1405-1408 ◽  
Author(s):  
Francesca Sperotto ◽  
Giorgio Cuffaro ◽  
Sara Brachi ◽  
Mara Seguso ◽  
Francesco Zulian

Objective.The role of antinuclear antibodies (ANA) in children has still to be elucidated. The aim of our study was to evaluate the prevalence and persistence of ANA in schoolchildren during the puberty switch, and the possible relationship with chronic noninflammatory musculoskeletal pain (MSP).Methods.Children aged 8–13 years and attending 4 public schools underwent a clinical examination, focusing on pubertal stage and presence of chronic noninflammatory MSP. Laboratory tests to determine the autoantibody-profile were also performed. Subjects with ANA positivity (titer ≥ 1:80) and/or chronic noninflammatory MSP were re-evaluated 3 years later.Results.Two hundred sixty-one subjects enrolled in the study and 12.3% were ANA-positive, equally distributed in terms of sex and pubertal status. Three years later, in the group of patients studied for chronic noninflammatory MSP (n = 67), ANA positivity significantly increased from 13.4% to 44.8%. In the ANA-positive cohort at baseline (n = 28), 92.9% of subjects were confirmed as being ANA-positive with a significantly increased titer. No association between ANA positivity and chronic noninflammatory MSP was found.Conclusion.ANA prevalence and titers increase during puberty, especially in females, but have no relationship with chronic noninflammatory MSP. This finding may be related to the complex hormonal changes during the puberty switch period and opens new insights into autoimmunity.


2002 ◽  
Vol 195 (9) ◽  
pp. 1167-1174 ◽  
Author(s):  
Silvia Bolland ◽  
Young-Sun Yim ◽  
Katalin Tus ◽  
Edward K. Wakeland ◽  
Jeffrey V. Ravetch

FcγRIIB is a potent lupus susceptibility gene as demonstrated by the observation that mice deficient in this molecule develop spontaneous antinuclear antibodies (ANA) and fatal glomerulonephritis when on the C57BL/6 background. To determine the mechanisms underlying the epistasis displayed by this gene we have constructed hybrids between FcγRIIB−/− and the systemic lupus erythematosus (SLE) modifiers yaa and lpr and the susceptibility locus Sle1. Sle1 and B6.RIIB−/− are both physically and functionally coupled; compound heterozygotes of Sle1 and B6.RIIB−/− develop significant disease, while single heterozygotes display no evidence of autoimmunity or disease, indicating that these genes lie on the same genetic pathway resulting in the loss of tolerance to nuclear antigens. However, the generation of ANA in itself is insufficient to account for the severity of autoimmune disease in this model, as demonstrated by analysis of yaa and lpr hybrids. Thus, B6.RIIB−/−/lpr mice are protected from disease progression, despite equivalent titers of ANA. In contrast, B6.RIIB−/−/yaa mice have significantly enhanced disease despite reduced ANA titers. Yaa modifies the specificity and thus the pathogenicity of the B6. RIIB−/− ANA, by converting them to antinucleolar antibodies. In addition to these known modifier pathways, we have discovered two novel, recessive loci contributed by the C57BL/6 genome that are required for the ANA phenotype, further indicating the epistatic properties of this SLE model.


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