Arraying Autoantibodies in SLE – Lessons Learned

Wang, L.; Mohan, Chandra; Li, Quan-Zhen

doi:10.2174/1566524015666150630124649

Cited by 10 publications

(8 citation statements)

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“…There are some obvious advantages of the autoantigen array over the conventional ANA detection methods such as indirect immunofluorescence (IF) and ELISA [19] . Use of the aforementioned conventional methods to analyze multiple antibodies in multiple samples may incur substantial cost, time, manpower, and even the serum samples.…”

Section: Autoantigen Microarray: Principle and Methodologymentioning

confidence: 99%

Autoantigen Microarray for High-Throughput Autoantibody Profiling in Systemic Lupus Erythematosus

Zhu

Luo

Yan

et al. 2015

Genomics, Proteomics &Amp; Bioinformatics

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Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by the production of autoantibodies to a broad range of self-antigens. Profiling the autoantibody repertoire using array-based technology has emerged as a powerful tool for the identification of biomarkers in SLE and other autoimmune diseases. Proteomic microarray has the capacity to hold large number of self-antigens on a solid surface and serve as a high-throughput screening method for the determination of autoantibody specificities. The autoantigen arrays carrying a wide variety of self-antigens, such as cell nuclear components (nucleic acids and associated proteins), cytoplasmic proteins, phospholipid proteins, cell matrix proteins, mucosal/secreted proteins, glomeruli, and other tissue-specific proteins, have been used for screening of autoantibody specificities associated with different manifestations of SLE. Arrays containing synthetic peptides and molecular modified proteins are also being utilized for identification of autoantibodies targeting to special antigenic epitopes. Different isotypes of autoantibodies, including IgG, IgM, IgA, and IgE, as well as other Ig subtypes, can be detected simultaneously with multi-color labeled secondary antibodies. Serum and plasma are the most common biologic materials for autoantibody detection, but other body fluids such as cerebrospinal fluid, synovial fluid, and saliva can also be a source of autoantibody detection. Proteomic microarray as a multiplexed high-throughput screening platform is playing an increasingly-important role in autoantibody diagnostics. In this article, we highlight the use of autoantigen microarrays for autoantibody exploration in SLE.

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Section: Autoantigen Microarray: Principle and Methodologymentioning

confidence: 99%

Autoantigen Microarray for High-Throughput Autoantibody Profiling in Systemic Lupus Erythematosus

Zhu

Luo

Yan

et al. 2015

Genomics, Proteomics &Amp; Bioinformatics

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“…Diverse dysregulation in innate [1,2,3] and adaptive [4,5] immune systems has been found in patients with systemic lupus erythematosus (SLE). These kinds of immune dysregulations stimulate protean autoantibody productions [6,7] and chronic immune-mediated inflammation [1,2,3,4]. Aging is defined as the physiologically progressive degeneration and decay of somatic tissues/organs and immune systems (immunosenescence).…”

Section: Introductionmentioning

confidence: 99%

Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking “Inflammaging” in Patients with Systemic Lupus Erythematosus

Tsai

Shen

Liao

et al. 2019

IJMS

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Systemic lupus erythematosus (SLE) is an archetype of systemic autoimmune disease, characterized by the presence of diverse autoantibodies and chronic inflammation. There are multiple factors involved in lupus pathogenesis, including genetic/epigenetic predisposition, sexual hormone imbalance, environmental stimulants, mental/psychological stresses, and undefined events. Recently, many authors noted that “inflammaging”, consisting of immunosenescence and inflammation, is a common feature in aging people and patients with SLE. It is conceivable that chronic oxidative stresses originating from mitochondrial dysfunction, defective bioenergetics, abnormal immunometabolism, and premature telomere erosion may accelerate immune cell senescence in patients with SLE. The mitochondrial dysfunctions in SLE have been extensively investigated in recent years. The molecular basis of normoglycemic metabolic syndrome has been found to be relevant to the production of advanced glycosylated and nitrosative end products. Besides, immunosenescence, autoimmunity, endothelial cell damage, and decreased tissue regeneration could be the results of premature telomere erosion in patients with SLE. Herein, the molecular and cellular bases of inflammaging and cardiovascular complications in SLE patients will be extensively reviewed from the aspects of mitochondrial dysfunctions, abnormal bioenergetics/immunometabolism, and telomere/telomerase disequilibrium.

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“…Systemic lupus erythematosus (SLE) is a typical autoimmune disease with abundant production of autoantibodies [ 1 ]. Through the binding of antigen and antibody, the immune complexes develop and deposit in various blood vessels, leading to multiorgans or systems involvement [ 2 , 3 ], which severely disturb the quality of life of patients [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

CXCL13 Promotes Proliferation of Mesangial Cells by Combination with CXCR5 in SLE

Zhu

et al. 2016

Journal of Immunology Research

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As a CXC subtype member of the chemokine superfamily, CXCL13 is considered to be involved in systemic lupus erythematosus (SLE), especially in lupus nephritis (LN). To determine the effect of CXCL13 on SLE and explore the potential mechanisms, we tested serum concentrations of CXCL13 in patients and healthy individuals and found that CXCL13 expression was high in SLE patients especially in LN patients. When we treated human renal mesangial cells (HRMCs) in vitro with recombinant human CXCL13, the cell proliferation was accelerated, which was tested by Cell Counting Kit-8 assay and flow cytometry. Western blot and immunofluorescence assay revealed that CXCL13 would lead to phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). However, the effect was weakened after the silence of CXCR5. The results of our study elaborated that high expression of CXCL13 could be involved in the pathogenesis of LN.

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Arraying Autoantibodies in SLE – Lessons Learned

Cited by 10 publications

References 0 publications

Autoantigen Microarray for High-Throughput Autoantibody Profiling in Systemic Lupus Erythematosus

Autoantigen Microarray for High-Throughput Autoantibody Profiling in Systemic Lupus Erythematosus

Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking “Inflammaging” in Patients with Systemic Lupus Erythematosus

CXCL13 Promotes Proliferation of Mesangial Cells by Combination with CXCR5 in SLE

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