Clinical evaluation of total and high-avidity anti-dsDNA antibody assays for the diagnosis of systemic lupus erythematosus

Yuan, Weiru; Cao, Hua; Wan, Ping; Shi, Ruihan; Zhou, Shu; Zheng, Jie

doi:10.1177/0961203319877243

Cited by 10 publications

(4 citation statements)

References 39 publications

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“…Similar to the previous studies, miR-101-3p expression was markedly reduced in SLE in the current study. To date, SLE diagnosis is supported by a variety of indices including anti-dsDNA, ESR, CRP, IgG and C3 (33)(34)(35)(36). Reduced expression of miR-98 is found to be associated with anti-dsDNA and SLEDAI in SLE PBMCs (37) while miR-203 expression is negatively associated with ESR and CRP in patients with SLE (38).…”

Section: Discussionmentioning

confidence: 99%

miR‑101‑3p negatively regulates inflammation in systemic lupus erythematosus via MAPK1 targeting and inhibition of the NF‑κB pathway

Zhao

Wang

et al. 2021

Mol Med Rep

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Systemic lupus erythematosus (SLE) is an autoimmune disease often used as a model in genomics research. The downregulation of microRNA-101-3p (miR-101-3p) participates in the progression of SLE, although the underlying mechanisms remain to be elucidated. The present study aimed to evaluate the specific roles of miR-101-3p in the SLE inflammatory response and its potential mechanisms. Reverse transcription-quantitative (RT-q) PCR was used to profile miR-101-3p expression in the peripheral blood mononuclear cells (PBMCs) from 40 female patients with SLE and 20 female healthy volunteers. The interactions between miR-101-3p and MAPK1 were identified and evaluated using dual-luciferase reporter and RNA pull-down assays. The levels of IL-10 and IFN-γ were evaluated by enzyme-linked immunosorbent assay. The expression of NF-κB p65 and phosphorylated IκBα were evaluated using western blotting. miR-101-3p expression was demonstrated to be downregulated in SLE PBMCs. miR-101-3p negatively regulated IL-10 and IFN-γ expression in SLE samples and was demonstrated to target MAPK1. Increases in MAPK1 expression eliminated miR-101-3p inhibition of IL-10 and IFN-γ. MAPK1 activated the NF-κB pathway in SLE PBMCs and this activation was inhibited when miR-101-3p was overexpressed. In addition, treatment with BAY11-7085 (NF-κB activator) was demonstrated to reverse the inhibitory effects of miR-101-3p expression on both IL-10 and IFN-γ in SLE PBMCs. BAY11-7082 also markedly reduced MAPK1-induced increases in IL-10 and IFN-γ in SLE PBMCs. miR-101-3p overexpression attenuated the inflammatory response in SLE PBMCs by inhibiting the expression of MAPK1 and blocking the NF-κB pathway. The results revealed a novel regulatory mechanism in SLE inflammation and offer a new direction for the development of SLE treatments.

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Section: Discussionmentioning

confidence: 99%

miR‑101‑3p negatively regulates inflammation in systemic lupus erythematosus via MAPK1 targeting and inhibition of the NF‑κB pathway

Zhao

Wang

et al. 2021

Mol Med Rep

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“…On the other hand, the avidity of the antigen-antibody interaction is also associated with the severity of autoimmune diseases [77,78]. In addition, avidity is a parameter that directly influences immunodiagnostic reactions, including avidity measurements being used to assess the stage of a given pathology [79][80][81][82][83].…”

Section: Affinity and Aviditymentioning

confidence: 99%

IgY Antibodies from Birds: A Review on Affinity and Avidity

Pacheco,

Nogueira,

Venancio

2023

Animals

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IgY antibodies are found in the blood and yolk of eggs. Several studies show the feasibility of utilising IgY for immunotherapy and immunodiagnosis. These antibodies have been studied because they fulfil the current needs for reducing, replacing, and improving the use of animals. Affinity and avidity represent the strength of the antigen–antibody interaction and directly influence antibody action. The aim of this review was to examine the factors that influence the affinity and avidity of IgY antibodies and the methodologies used to determine these variables. In birds, there are few studies on the maturation of antibody affinity and avidity, and these studies suggest that the use of an adjuvant-type of antigen, the animal lineage, the number of immunisations, and the time interfered with the affinity and avidity of IgY antibodies. Regarding the methodologies, most studies use chaotropic agents to determine the avidity index. Studies involving the solution phase and equilibrium titration reactions are also described. These results demonstrate the need for the standardisation of methodologies for the determination of affinity and avidity so that further studies can be performed to optimise the production of high avidity IgY antibodies.

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“…Antidouble-stranded DNA (anti-dsDNA) autoantibodies play a pivotal role in the diagnosis and follow-up of SLE [1][2][3] and are related to the development of lupus nephritis. 4 5 The 2019 European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR) criteria for classifying SLE include positive values for SLE-specific antibodies, such as anti-dsDNA autoantibodies, as the criterion with the highest weight in the immunology domains.…”

Section: Introductionmentioning

confidence: 99%

Longitudinal study of patients with discrepant results in CLIFT and a solid-phase dsDNA antibody assay: does a gold standard dsDNA assay exist?

Trujillo Aguilera,

Bernardo Serrano,

Navas

et al. 2023

Lupus Sci Med

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ObjectiveAntidouble-stranded DNA (dsDNA) antibodies are essential for diagnosis and follow-up of systemic lupus erythematous (SLE). To ensure the best diagnostic approach, most healthcare laboratories opt for a combination of highly sensitive methods, such as solid-phase immunoassays, and highly specific methods, such as theCrithidia luciliaeindirect immunofluorescence test (CLIFT). Even so, discordant results are common, thus hindering the diagnostic process. Therefore, this study aimed to characterise a cohort of patients with discrepant results for a dsDNA fluorescence enzyme immunoassay (FEIA) and CLIFT during 2016–2018 and to follow patients up until December 2021.MethodsWe performed an observational, longitudinal and retrospective study on 417 samples from 257 patients who had been referred for suspected connective tissue diseases or followed up after diagnosis. All of them were positive for antinuclear antibodies (ANAs) using an indirect immunofluorescence assay (IFA) on Hep-2 cells, the entry criterion in our laboratory, and positive for FEIA dsDNA. Samples were then tested with CLIFT according to our routine protocol, which includes CLIFT testing after FEIA dsDNA results ≥10 UI/ml. After the assessment of data quality, the final analysis was based on 222 patients.ResultsEighty-three patients (37.4%) had positive results in both tests and met the diagnostic criteria for SLE. However, 139 patients (62.6%) had discrepant results (FEIA+, CLIFT–). Of these, 58 patients (41.7%) had a diagnosis of SLE, with 47 (33.8%) having been previously diagnosed and under treatment. The remaining 11 patients (7.9%) had a new diagnosis of SLE, which was made up within 4 years of the initial screening. A total of 81 of the 139 patients (57.5%) with discrepant results did not meet lupus criteria during the follow-up period.ConclusionsThe study showed that CLIFT could be negative in both treated and newly diagnosed SLE, thus underlining the importance of follow-up of dsDNA-positive results using solid-phase tests. Therefore, quantitative tests such as FEIA could add value to the diagnosis and management of patients with suspected SLE.

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Clinical evaluation of total and high-avidity anti-dsDNA antibody assays for the diagnosis of systemic lupus erythematosus

Cited by 10 publications

References 39 publications

miR‑101‑3p negatively regulates inflammation in systemic lupus erythematosus via MAPK1 targeting and inhibition of the NF‑κB pathway

miR‑101‑3p negatively regulates inflammation in systemic lupus erythematosus via MAPK1 targeting and inhibition of the NF‑κB pathway

IgY Antibodies from Birds: A Review on Affinity and Avidity

Longitudinal study of patients with discrepant results in CLIFT and a solid-phase dsDNA antibody assay: does a gold standard dsDNA assay exist?

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