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Antibodies, Volume 5, Issue 2 (June 2016)

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Open AccessReview
The Significance of Anti-Beta-2-Glycoprotein I Antibodies in Antiphospholipid Syndrome
Antibodies 2016, 5(2), 16; https://doi.org/10.3390/antib5020016
Received: 26 April 2016 / Revised: 24 May 2016 / Accepted: 3 June 2016 / Published: 8 June 2016
Cited by 9 | Viewed by 1965 | PDF Full-text (196 KB) | HTML Full-text | XML Full-text
Abstract
Antiphospholipid syndrome (APS) is a thrombophilic disorder that classically presents with vascular thrombosis and/or obstetric complications. APS is associated with antiphospholipid antibodies: a heterogeneous group of autoantibodies that are directed against membrane phospholipids in complex with phospholipid-binding proteins. Beta-2-glycoprotein I (B2GPI) binds anionic [...] Read more.
Antiphospholipid syndrome (APS) is a thrombophilic disorder that classically presents with vascular thrombosis and/or obstetric complications. APS is associated with antiphospholipid antibodies: a heterogeneous group of autoantibodies that are directed against membrane phospholipids in complex with phospholipid-binding proteins. Beta-2-glycoprotein I (B2GPI) binds anionic phospholipids and is considered to be the predominant antigen in APS and antibodies against B2GPI (anti-B2GPI) are recognised in the laboratory criteria for APS diagnosis. This review focuses on the part played by anti-B2GPI in the pathogenesis of APS, their associations with different clinical phenotypes of the disorder and new avenues for refining the diagnostic potential of anti-B2GPI testing. Full article
(This article belongs to the Special Issue Antiphospholipid Antibodies and Syndrome) Printed Edition available
Open AccessReview
Antiphospholipid Antibodies: Their Origin and Development
Antibodies 2016, 5(2), 15; https://doi.org/10.3390/antib5020015
Received: 28 April 2016 / Revised: 18 May 2016 / Accepted: 19 May 2016 / Published: 2 June 2016
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Abstract
Antiphospholipid antibodies (aPL) are a hallmark of the antiphospholipid syndrome (APS), which is the most commonly acquired thrombophilia. To date there is consensus that aPL cause the clinical manifestations of this potentially devastating disorder. However, there is good evidence that not all aPL [...] Read more.
Antiphospholipid antibodies (aPL) are a hallmark of the antiphospholipid syndrome (APS), which is the most commonly acquired thrombophilia. To date there is consensus that aPL cause the clinical manifestations of this potentially devastating disorder. However, there is good evidence that not all aPL are pathogenic. For instance, aPL associated with syphilis show no association with the manifestations of APS. While there has been intensive research on the pathogenetic role of aPL, comparably little is known about the origin and development of aPL. This review will summarize the current knowledge and understanding of the origin and development of aPL derived from animal and human studies. Full article
(This article belongs to the Special Issue Antiphospholipid Antibodies and Syndrome) Printed Edition available
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Open AccessArticle
A Clinical Approach for Defining the Threshold between Low and Medium Anti-Cardiolipin Antibody Levels for QUANTA Flash Assays
Antibodies 2016, 5(2), 14; https://doi.org/10.3390/antib5020014
Received: 14 March 2016 / Revised: 15 May 2016 / Accepted: 16 May 2016 / Published: 25 May 2016
Cited by 2 | Viewed by 2191 | PDF Full-text (499 KB) | HTML Full-text | XML Full-text
Abstract
The threshold between low and medium antibody levels for anticardiolipin (aCL) and anti-β2 glycoprotein I antibodies (aβ2GPI) for the diagnosis of antiphospholipid syndrome (APS) remains a matter of discussion. Our goal was to create a protocol for determining the low/medium antibody cut-off for [...] Read more.
The threshold between low and medium antibody levels for anticardiolipin (aCL) and anti-β2 glycoprotein I antibodies (aβ2GPI) for the diagnosis of antiphospholipid syndrome (APS) remains a matter of discussion. Our goal was to create a protocol for determining the low/medium antibody cut-off for aCL antibody methods based on a clinical approach, and utilize it to establish the clinically-relevant low/medium threshold for QUANTA Flash aCL chemiluminescent immunoassay (CIA) results. The study included 288 samples from patients with primary APS (n = 70), secondary APS (n = 42), suspected APS (n = 36), systemic lupus erythematosus (SLE) without APS (n = 96) and other connective tissue diseases (n = 44). All samples were tested for IgG and IgM aCL antibodies with QUANTA Flash CIA, along with traditional enzyme-linked immunosorbent assays (ELISAs) (QUANTA Lite). The assay specific low/medium threshold for QUANTA Flash aCL IgG and IgM assays (i.e., the equivalent of 40 GPL and MPL units) was established as 95 and 31 chemiluminescent units (CU), respectively, based on clinical performance and comparison to QUANTA Lite ELISAs. Agreement between CIA and ELISA assay results improved substantially when the platform-specific low/medium antibody threshold was used, as compared to agreement obtained on results generated with the assay cutoff: Cohen’s kappa increased from 0.85 to 0.91 for IgG aCL, and from 0.59 to 0.75 for IgM aCL results. This study describes a clinical approach for establishing the low/medium antibody threshold for aPL antibody assays, and successfully employs it to define 95 and 31 CU, respectively, as the low/medium cut point for QUANTA Flash aCL IgG and IgM results. This study can serve as a model for labs wishing to establish the appropriate low/medium aPL antibody threshold when implementing new aPL antibody assays. Full article
(This article belongs to the Special Issue Antiphospholipid Antibodies and Syndrome) Printed Edition available
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Open AccessArticle
Binding Analysis of Human Immunoglobulin G as a Zinc-Binding Protein
Antibodies 2016, 5(2), 13; https://doi.org/10.3390/antib5020013
Received: 4 March 2016 / Revised: 28 April 2016 / Accepted: 12 May 2016 / Published: 19 May 2016
Cited by 2 | Viewed by 1796 | PDF Full-text (1317 KB) | HTML Full-text | XML Full-text
Abstract
Human immunoglobulin G (IgG) binding with zinc ions was examined using zinc ions immobilized on chelating Sepharose beads (Zn-beads). Human IgG bound to Zn-beads but not to Sepharose beads (control beads). Mouse, rat, bovine and equine IgGs also bound to Zn-beads, similar to [...] Read more.
Human immunoglobulin G (IgG) binding with zinc ions was examined using zinc ions immobilized on chelating Sepharose beads (Zn-beads). Human IgG bound to Zn-beads but not to Sepharose beads (control beads). Mouse, rat, bovine and equine IgGs also bound to Zn-beads, similar to human IgG. The human IgG F(c) fragment showed zinc ion–binding activity whereas the Fab fragment did not. Ethylenediaminetetraacetic acid (EDTA)-treated Zn-beads no longer bound human IgG; however, washing the beads, followed by the addition of zinc ions, restored the binding activity towards human IgG. Zn-beads saturated with human fibrinogen could bind human IgG, and Zn-beads saturated with human IgG could bind fibrinogen. These results suggest that animal IgGs, including human, specifically bind zinc ions, probably through a zinc-binding site in the F(c) fragment and not in the Fab fragment. In addition, IgG and fibrinogen interact with each other and/or bind zinc ions through different mechanisms. Full article
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Open AccessReview
β2GP1, Anti-β2GP1 Antibodies and Platelets: Key Players in the Antiphospholipid Syndrome
Antibodies 2016, 5(2), 12; https://doi.org/10.3390/antib5020012
Received: 5 April 2016 / Revised: 26 April 2016 / Accepted: 26 April 2016 / Published: 6 May 2016
Cited by 5 | Viewed by 3334 | PDF Full-text (885 KB) | HTML Full-text | XML Full-text
Abstract
Anti-beta 2 glycoprotein 1 (anti-β2GP1) antibodies are commonly found in patients with autoimmune diseases such as the antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). Their presence is highly associated with increased risk of vascular thrombosis and/or recurrent pregnancy-related complications. Although [...] Read more.
Anti-beta 2 glycoprotein 1 (anti-β2GP1) antibodies are commonly found in patients with autoimmune diseases such as the antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE). Their presence is highly associated with increased risk of vascular thrombosis and/or recurrent pregnancy-related complications. Although they are a subtype of anti-phospholipid (APL) antibody, anti-β2GP1 antibodies form complexes with β2GP1 before binding to different receptors associated with anionic phospholipids on structures such as platelets and endothelial cells. β2GP1 consists of five short consensus repeat termed “sushi” domains. It has three interchangeable conformations with a cryptic epitope at domain 1 within the molecule. Anti-β2GP1 antibodies against this cryptic epitope are referred to as ‘type A’ antibodies, and have been suggested to be more strongly associated with both vascular and obstetric complications. In contrast, ‘type B’ antibodies, directed against other domains of β2GP1, are more likely to be benign antibodies found in asymptomatic patients and healthy individuals. Although the interactions between anti-β2GP1 antibodies, β2GP1, and platelets have been investigated, the actual targeted metabolic pathway(s) and/or receptor(s) involved remain to be clearly elucidated. This review will discuss the current understanding of the interaction between anti-β2GP1 antibodies and β2GP1, with platelet receptors and associated signalling pathways. Full article
(This article belongs to the Special Issue Antiphospholipid Antibodies and Syndrome) Printed Edition available
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Open AccessReview
Generating Recombinant Antibodies to Membrane Proteins through Phage Display
Antibodies 2016, 5(2), 11; https://doi.org/10.3390/antib5020011
Received: 25 March 2016 / Revised: 21 April 2016 / Accepted: 21 April 2016 / Published: 2 May 2016
Cited by 4 | Viewed by 3502 | PDF Full-text (1974 KB) | HTML Full-text | XML Full-text
Abstract
One of the most important classes of proteins in terms of drug targets is cell surface membrane proteins, and yet it is a challenging set of proteins for generating high-quality affinity reagents. In this review, we focus on the use of phage libraries, [...] Read more.
One of the most important classes of proteins in terms of drug targets is cell surface membrane proteins, and yet it is a challenging set of proteins for generating high-quality affinity reagents. In this review, we focus on the use of phage libraries, which display antibody fragments, for generating recombinant antibodies to membrane proteins. Such affinity reagents generally have high specificity and affinity for their targets. They have been used for cell staining, for promoting protein crystallization to solve three-dimensional structures, for diagnostics, and for treating diseases as therapeutics. We cover publications on this topic from the past 10 years, with a focus on the various formats of membrane proteins for affinity selection and the diverse affinity selection strategies used. Lastly, we discuss the challenges faced in this field and provide possible directions for future efforts. Full article
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Open AccessCorrection
Correction: Cytokines in the Germinal Center Niche Antibodies 2016, 5(1), 5
Antibodies 2016, 5(2), 10; https://doi.org/10.3390/antib5020010
Received: 17 November 2015 / Revised: 27 January 2016 / Accepted: 27 January 2016 / Published: 27 April 2016
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Abstract
The following corrections should be made to the references and bibliography of the published paper [1]:[...] Full article
Open AccessReview
Autoantibodies in Neuropsychiatric Disorders
Antibodies 2016, 5(2), 9; https://doi.org/10.3390/antib5020009
Received: 26 January 2016 / Revised: 1 April 2016 / Accepted: 6 April 2016 / Published: 21 April 2016
Cited by 6 | Viewed by 3470 | PDF Full-text (460 KB) | HTML Full-text | XML Full-text
Abstract
Little is known about the etiology of neuropsychiatric disorders. The identification of autoantibodies targeting the N-methyl-d-aspartate receptor (NMDA-R), which causes neurological and psychiatric symptoms, has reinvigorated the hypothesis that other patient subgroups may also suffer from an underlying autoimmune condition. [...] Read more.
Little is known about the etiology of neuropsychiatric disorders. The identification of autoantibodies targeting the N-methyl-d-aspartate receptor (NMDA-R), which causes neurological and psychiatric symptoms, has reinvigorated the hypothesis that other patient subgroups may also suffer from an underlying autoimmune condition. In recent years, a wide range of neuropsychiatric diseases and autoantibodies targeting ion-channels or neuronal receptors including NMDA-R, voltage gated potassium channel complex (VGKC complex), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA-R), γ-aminobutyric acid receptor (GABA-R) and dopamine receptor (DR) were studied and conflicting reports have been published regarding the seroprevalence of these autoantibodies. A clear causative role of autoantibodies on psychiatric symptoms has as yet only been shown for the NMDA-R. Several other autoantibodies have been related to the presence of certain symptoms and antibody effector mechanisms have been proposed. However, extensive clinical studies with large multicenter efforts to standardize diagnostic procedures for autoimmune etiology and animal studies are needed to confirm the pathogenicity of these autoantibodies. In this review, we discuss the current knowledge of neuronal autoantibodies in the major neuropsychiatric disorders: psychotic, major depression, autism spectrum, obsessive-compulsive and attention-deficit/hyperactivity disorders. Full article
(This article belongs to the Special Issue Auto-Antibody and Autoimmune Disease)
Open AccessReview
Epigenetic Regulation of Innate Immunity by microRNAs
Antibodies 2016, 5(2), 8; https://doi.org/10.3390/antib5020008
Received: 17 December 2015 / Revised: 16 March 2016 / Accepted: 16 March 2016 / Published: 1 April 2016
Cited by 3 | Viewed by 2379 | PDF Full-text (733 KB) | HTML Full-text | XML Full-text
Abstract
The innate immune response, which is usually referred to as the first line of defense, protects the hosts against pathogenic micro-organisms. Some of the biomolecules released from the pathogens, such as proteins, lipoproteins and nucleic acids, which are collectively termed as pathogen-associated molecular [...] Read more.
The innate immune response, which is usually referred to as the first line of defense, protects the hosts against pathogenic micro-organisms. Some of the biomolecules released from the pathogens, such as proteins, lipoproteins and nucleic acids, which are collectively termed as pathogen-associated molecular patterns (PAMPs), elicit signaling mechanisms that trigger immune responses in the hosts. Pathogen recognition receptors (PRRs) on the host cells recognize these PAMPs and initiate intracellular signaling through toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and other pathways which induce production of pro-inflammatory cytokines and type I interferons. Recently, different members of tripartite motif containing proteins (TRIM) family of proteins were identified to intercept and regulate these cellular pathways. Specific targets of TRIM proteins have been identified and their molecular mechanisms were unraveled and identified unique domains involved in protein-protein interactions. Though innate immunity represents a tight and well conserved immune system in the host, gene expression in innate immunity was identified to be influenced by several epigenetic mechanisms including regulation by microRNAs (miRNAs). In this review, we present critical analysis of the findings on the identification of specific miRNAs that modulate expression of target genes involved in the regulation of innate immunity. Full article
(This article belongs to the Special Issue Intracellular Innate Immunity of Antibodies)
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Open AccessArticle
Development and Characterization of New Species Cross-Reactive Anti-Sialoadhesin Monoclonal Antibodies
Antibodies 2016, 5(2), 7; https://doi.org/10.3390/antib5020007
Received: 25 January 2016 / Revised: 3 March 2016 / Accepted: 14 March 2016 / Published: 23 March 2016
Cited by 2 | Viewed by 2385 | PDF Full-text (1980 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Sialoadhesin (Sn) is a surface receptor expressed on a subset of macrophages in steady state conditions. During inflammation and diseases, Sn is highly upregulated on macrophages and blood monocytes. Therefore, therapies using monoclonal antibodies (mAbs) to target Sn-positive (Sn+) cells are [...] Read more.
Sialoadhesin (Sn) is a surface receptor expressed on a subset of macrophages in steady state conditions. During inflammation and diseases, Sn is highly upregulated on macrophages and blood monocytes. Therefore, therapies using monoclonal antibodies (mAbs) to target Sn-positive (Sn+) cells are a potential strategy for targeted treatment. It has been shown that Sn internalizes after binding with a mAb, though it is not clear whether this is species-specific. In this study, new Sn-specific mAbs were developed and analyzed for cross-reactivity between species. In addition, the newly developed mAbs were compared to mAbs used in previous research for their epitope recognition and other Sn-specific characteristics. Both species-specific and cross-reactive antibodies could be identified. Furthermore, sialic acid-binding of red blood cells (RBC) could be inhibited with mAbs recognizing different epitopes and all mAb showed internalization of Sn. The newly developed mAbs can be used as novel tools for Sn research and further analysis of Sn internalization in different species. Full article
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