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Autoantibodies - Top 30 Publications

Untargeted screening for novel autoantibodies with prognostic value in first-episode psychosis.

Immunological and inflammatory reactions have been suggested to have a role in the development of schizophrenia, a hypothesis that has recently been supported by genetic data. The aim of our study was to perform an unbiased search for autoantibodies in patients with a first psychotic episode, and to explore the association between any seroreactivity and the development of a Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV) disorder characterized by chronic or relapsing psychotic symptoms. We collected plasma samples from 53 patients when they were treated for their first-episode psychosis, and 41 non-psychotic controls, after which the patients were followed for a mean duration of 7 years. Thirty patients were diagnosed with schizophrenia, delusional disorder, schizoaffective disorder, bipolar disorder or a long-term unspecified nonorganic psychosis during follow-up, whereas 23 patients achieved complete remission. At the end of follow-up, plasma samples were analyzed for IgG reactivity to 2304 fragments of human proteins using a multiplexed affinity proteomic technique. Eight patient samples showed autoreactivity to the N-terminal fragment of the PAGE (P antigen) protein family (PAGE2B/PAGE2/PAGE5), whereas no such autoreactivity was seen among the controls. PAGE autoreactivity was associated with a significantly increased risk of being diagnosed with schizophrenia during follow-up (odds ratio 6.7, relative risk 4.6). An immunohistochemistry analysis using antisera raised against the N-terminal fragment stained an unknown extracellular target in human cortical brain tissue. Our findings suggest that autoreactivity to the N-terminal portion of the PAGE protein family is associated with schizophrenia in a subset of patients with first-episode psychosis.

The autoimmune/inflammatory syndrome induced by adjuvants (ASIA)/Shoenfeld's syndrome: descriptive analysis of 300 patients from the international ASIA syndrome registry.

The autoimmune/inflammatory syndrome induced by adjuvants (ASIA) is a recently identified condition in which the exposure to an adjuvant leads to an aberrant autoimmune response. We aimed to summarize the results obtained from the ASIA syndrome registry up to December 2016, in a descriptive analysis of 300 cases of ASIA syndrome, with a focus on the adjuvants, the clinical manifestations, and the relationship with other autoimmune diseases. A Web-based registry, based on a multicenter international study, collected clinical and laboratory data in a form of a questionnaire applied to patients with ASIA syndrome. Experts in the disease validated all cases independently. A comparison study regarding type of adjuvants and differences in clinical and laboratory findings was performed. Three hundred patients were analyzed. The mean age at disease onset was 37 years, and the mean duration of time latency between adjuvant stimuli and development of autoimmune conditions was 16.8 months, ranging between 3 days to 5 years. Arthralgia, myalgia, and chronic fatigue were the most frequently reported symptoms. Eighty-nine percent of patients were also diagnosed with another defined rheumatic/autoimmune condition. The most frequent autoimmune disease related to ASIA syndrome was undifferentiated connective tissue disease (UCTD). ASIA syndrome is associated with a high incidence of UCTD and positive anti-nuclear antibodies (ANA) test. Clinical and laboratory features differ from the type of adjuvant used. These findings may contribute to an increased awareness of ASIA syndrome and help physicians to identify patients at a greater risk of autoimmune diseases following the exposure to vaccines and other adjuvants. The ASIA syndrome registry provides a useful tool to systematize this rare condition.

The performance of different anti-dsDNA autoantibodies assays in Chinese systemic lupus erythematosus patients.

To compare the performance of different commercial anti-dsDNA autoantibody assays, including multiplex-based immunoassay (Bio-Plex), Farr radioimmunoassay (Farr), ELISA, chemiluminescent immunoassay (CLIA), and Crithidia Luciliae indirect immunofluorescence test (CLIFT) in Chinese patients with systemic lupus erythematosus (SLE). SLE patients (n = 119) as well as healthy controls (n = 200) and disease controls (n = 100) were recruited, and serum anti-dsDNA autoantibodies were detected by Bio-Plex, Farr, two ELISA assays (Medical & Biological Laboratories-ELISA, EUROIMMU-ELISA), CLIA, and a standard CLIFT. The correlation of anti-dsDNA autoantibody levels to SLE disease activity was calculated, and the specificity and sensitivity of these methods were measured by receiver-operator characteristic (ROC) curve analysis. In ROC curve analysis, Bio-Plex showed the largest area under the curve (AUC) over other assays. Cutoff adjustment according to ROC enhanced the performance of all quantitative assays. Overall, Bio-Plex and CLIFT have higher specificity (>90.00%). ELISA and CLIA results are correlated with disease activity, and Bio-Plex results have the strongest correlation with SLEDAI score and active renal involvement. Bio-Plex assay has better overall performance in anti-dsDNA detection over Farr, ELISA, and CLIA methods in Chinese SLE patients.

Anastrozole-induced Autoimmune Hepatitis: A Rare Complication of Breast Cancer Therapy.

Autoimmune hepatitis (AIH) is an extremely rare complication of anastrozole therapy. It presents with elevated liver function tests. The diagnosis is established by detecting high titers of autoantibodies such as antinuclear antibodies, anti-smooth muscle antibodies, and elevated immunoglobulins. It is confirmed with a liver biopsy showing interface rosetting and an increased number of plasma cells. Early diagnosis of anastrozole-induced AIH is important because it allows anastrozole to be discontinued and immunomodulatory treatment to be promptly initiated.

Development of autoantibodies precedes clinical manifestations of autoimmune diseases: A comprehensive review.

The etiology of autoimmune diseases is due to a combination of genetic predisposition and environmental factors that alter the expression of immune regulatory genes through various mechanisms including epigenetics. Both humoral and cellular elements of the adaptive immune system play a role in the pathogenesis of autoimmune diseases and the presence of autoantibodies have been detected in most but not all autoimmune diseases before the appearance of clinical symptoms. In some cases, the presence or levels of these autoantibodies portends not only the risk of developing a corresponding autoimmune disease, but occasionally the severity as well. This observation is intriguing because it suggests that we can, to some degree, predict who may or may not develop autoimmune diseases. However, the role of autoantibodies in the pathogenesis of autoimmune diseases, whether they actually affect disease progression or are merely an epiphenomenon is still not completely clear in many autoimmune diseases. Because of these gaps in our knowledge, the ability to accurately predict a future autoimmune disease can only be considered a relative risk factor. Importantly, it raises the critical question of defining other events that may drive a patient from a preclinical to a clinical phase of disease.

Emerging technologies in autoantibody testing for rheumatic diseases.

Testing for the presence of antinuclear antibodies (ANAs) is a key step in the diagnosis of systemic lupus erythematosus (SLE) and other systemic autoimmune rheumatic diseases (SARD). The standard slide-based indirect immunofluorescence (IIF) test is widely used, but is limited by a relative lack of specificity for SLE and not all SARD-ANAs are detected. Alternative immunoassays that might offer enhanced diagnostic and prognostic information have evolved, and some of these have entered clinical practice. This review summarizes the current state of ANA testing and multiplex techniques for detecting other autoantibodies, the possibility of point-of-care testing, and approaches for applications in early disease stages.

The role of autoantibodies in the syndromes of orthostatic intolerance: a systematic review.

Orthostatic intolerance is defined as the provocation of symptoms upon standing, commonly caused by neurogenic orthostatic hypotension (OH) and postural tachycardia syndrome (POTS), the etiology for which has not been fully uncovered yet. Many reports have described the occurrence of dysautonomia, orthostatic intolerance and POTS following febrile illness, presumably viral and post-vaccine. Furthermore, patients with dysautonomia have higher rates of autoimmune disorders such as Hashimoto thyroiditis and SLE. Recent evidence has shown the presence of adrenergic and cholinergic receptor antibodies in patients with POTS and orthostatic hypotension. In patients with cholinergic receptor antibodies, higher titers correlate with the disease severity. Few reports have shown that immunomodulation therapy resulted in significant improvement in symptoms. In this article, we review the available literature correlating autoimmunity with orthostatic intolerance syndromes. Future studies are warranted to evaluate the prevalence of such antibodies and examine different treatment modalities in this sub group of patients.

Nitration of H2B histone elicits an immune response in experimental animals.

Histone H2B is an autoantigen that appears in circulation due to altered apoptosis/or insufficient clearance and is likely to be involved in the induction and progression of autoimmune diseases since modified-H2B is immunogenic. Our studies demonstrate that tyrosines of H2B histone spontaneously converts to free and nitrotyrosine bound protein in vivo. Commercially available H2B histone was modified with peroxynitrite in vitro. Modified H2B was found to be more immunogenic than native form in experimental animals. Furthermore, the sera of rabbits were analyzed for the native and modified forms of the H2B histone. The binding specificity of autoantibodies was characterized by competitive enzyme-linked immunosorbent assay (ELISA) and band shift assay. The free 3-nitrotyrosine in systemic lupus erythematosus sera was quantified by high-performance liquid chromatography. Peroxynitrite-modified H2B induced high titre antibodies as compared to native form which were directly proportional to the nitrotyrosine content. Furthermore, the induced antibodies showed specificity towards the immunogen and cross-reacted with tyrosine-nitrated proteins. ELISA showed preferential binding of induced anti-peroxynitrite modified H2B antibodies to modified H2B as compared to native H2B. The present study shows that peroxynitrite modification of self-antigen(s) generates neoepitopes capable of inducing modified-H2B autoantibodies in experimental animals.

Peptide mimetics of immunoglobulin A (IgA) and FcαRI block IgA-induced human neutrophil activation and migration.

The cross-linking of the IgA Fc receptor (FcαRI) by IgA induces release of the chemoattractant LTB4, thereby recruiting neutrophils in a positive feedback loop. IgA autoantibodies of patients with autoimmune blistering skin diseases therefore induce massive recruitment of neutrophils, resulting in severe tissue damage. To interfere with neutrophil mobilization and reduce disease morbidity, we developed a panel of specific peptides mimicking either IgA or FcαRI sequences. CLIPS technology was used to stabilize three-dimensional structures and to increase peptides' half-life. IgA and FcαRI peptides reduced phagocytosis of IgA-coated beads, as well as IgA-induced ROS production and neutrophil migration in in vitro and ex vivo (human skin experiments). Since topical application would be the preferential route of administration, Cetomacrogol cream containing an IgA CLIPS peptide was developed. In the presence of a skin permeation enhancer, peptides in this cream were shown to penetrate the skin, while not diffusing systemically. Finally, epitope mapping was used to discover sequences important for binding between IgA and FcαRI. In conclusion, a cream containing IgA or FcαRI peptide mimetics, which block IgA-induced neutrophil activation and migration in the skin may have therapeutic potential for patients with IgA-mediated blistering skin diseases. This article is protected by copyright. All rights reserved.

B-cells as therapeutic targets in neuro-inflammatory diseases.

B cells are an emerging therapeutic target in neuroinflammatory diseases. The anti-CD20 monoclonal antibody ocrelizumab was recently approved in the US as the first B-cell targeting immunomodulatory treatment for relapsing-remitting MS and primary progressive MS. In autoantibody-associated demyelinating syndromes such as neuromyelitis optica (NMO) and in myelin-oligodendrocyte-glycoprotein-(MOG)-autoantibody-associated encephalomyelitis, B-cells are a logical target based on the pathogenesis of these antibody-mediated disorders. Furthermore, B cells and autoantibodies are promising targets in a variety of autoantibody-associated encephalitis syndromes such as N-methyl-d-aspartate receptor (NMDAR)-antibody encephalitis.

B cells and their cytokine activities implications in human diseases.

B cells are the only cell type that can give rise to antibody-producing cells, and the only cell type whose selective depletion can, today, lead to an improvement of a wide range of immune-mediated inflammatory diseases, including disorders not primarily driven by autoantibodies. Here, I discuss this paradoxical observation, and propose that the capacity of B cells to act as cytokine-producing cells explains how they can control monocyte activity and subsequently disease pathogenesis. Together with current data on the effect of anti-CD20 B cell-depleting reagents in the clinic, this novel knowledge on B cell heterogeneity opens the way for novel safer and more efficient strategies to target B cells. The forthcoming identification of disease-relevant B cell subsets is awaited to permit their monitoring and specific targeting in a personalized medicine approach.

Detection of mucous membrane pemphigoid autoantibodies by full-length BP180 enzyme-linked immunosorbent assay.

Autoimmune Liver Disease in Children with Sickle Cell Disease.

To assess the incidence, clinical features, and outcome of autoimmune liver disease (AILD) in patients with sickle cell disease (SCD).

Autoimmunity and its association with regulatory T cells and B cell subsets in patients with common variable immunodeficiency.

Common variable immunodeficiency (CVID) is one of the most prevalent symptomatic primary immunodeficiencies (PIDs), which manifests a wide clinical variability such as autoimmunity, as well as T cell and B cell abnormalities.

Duration of maintenance therapy for ANCA-associated vasculitis: more questions than answers.

Potential Predictive Role of Lipid Peroxidation Markers for Type 2 Diabetes in the Tunisian Population.

We evaluated the potential clinical relevance of malondialdehyde (MDA) and autoantibodies to copper oxidized low-density lipoprotein (CuOx-LDL) in type 2 diabetes occurrence.

Appearance of anti-desmocollin 1 autoantibodies leading to a vegetative lesion in a pemphigus vulgaris patient.

Pemphigus is a group of autoimmune bullous diseases that is mainly classified into pemphigus vulgaris (PV) and pemphigus foliaceus.(1) PV is further subcategorized into a mucocutaneous type (with autoantibodies against desmoglein (Dsg) 3 and Dsg1) and a mucosal type (with autoantibodies against Dsg3 but not Dsg1) based on autoantibody profile and clinical features. Pemphigus vegetans (PVeg), a rare variant of PV, is characterized by vegetating lesions. However, the mechanism behind the occurrence of these elevated lesions remains unclear.(2) Recently, it was reported that anti-desmocollin (Dsc) 1 and Dsc3 autoantibodies were frequently detected and potentially pathogenic in PVeg.(3) Here we report a case of PV in which a vegetative plaque occurred during treatment accompanied by the elevation of anti-Dsc1 autoantibodies. This article is protected by copyright. All rights reserved.

Strategies to improve the efficiency of celiac disease diagnosis in the laboratory.

The demand for testing to detect celiac disease (CD) autoantibodies has increased, together with the cost per case diagnosed, resulting in the adoption of measures to restrict laboratory testing. We designed this study to determine whether opportunistic screening to detect CD-associated autoantibodies had advantages compared to efforts to restrict testing, and to identify the most cost-effective diagnostic strategy. We compared a group of 1678 patients in which autoantibody testing was restricted to cases in which the test referral was considered appropriate (G1) to a group of 2140 patients in which test referrals were not reviewed or restricted (G2). Two algorithms A (quantifying IgA and Tissue transglutaminase IgA [TG-IgA] in all patients), and B (quantifying only TG-IgA in all patients) were used in each group, and the cost-effectiveness of each strategy was calculated. TG-IgA autoantibodies were positive in 62 G1 patients and 69 G2 patients. Among those positive for tissue transglutaminase IgA and endomysial IgA autoantibodies, the proportion of patients with de novo autoantibodies was lower (p=0.028) in G1 (11/62) than in G2 (24/69). Algorithm B required fewer determinations than algorithm A in both G1 (2310 vs 3493; p<0.001) and G2 (2196 vs 4435; p<0.001). With algorithm B the proportion of patients in whom IgA was tested was lower (p<0.001) in G2 (29/2140) than in G1 (617/1678). The lowest cost per case diagnosed (4.63 euros/patient) was found with algorithm B in G2. We conclude that opportunistic screening has advantages compared to efforts in the laboratory to restrict CD diagnostic testing. The most cost-effective strategy was based on the use of an appropriate algorithm.

Synapsin-antibodies in psychiatric and neurological disorders: prevalence and clinical findings.

To study the prevalence of autoantibodies to synapsin in patients with psychiatric and neurological disorders and to describe clinical findings in synapsin antibody positive patients.

Decreased expression of miR-150, miR146a and miR424 in type 1 diabetic patients: Association with ongoing islet autoimmunity.

Recent studies revealed altered miRNAs profiling in patients with autoimmune diseases, including type 1 diabetes (T1D). Here, we conducted an observational study and examined the expression levels of these five miRNAs (miR-150,miR-146a,miR-424,miR-181a and miR-142-3P) in peripheral blood mononuclear cells (PBMCs) from T1D patients.

New answers to old conundrums: what antibodies, exosomes and inflammasomes bring to the conversation. Canadian National Transplant Research Program international summit report.

Antibody-mediated injury is a major cause of allograft dysfunction and loss. Antibodies to ABH(O) blood group antigens are classical mediators of ABO-incompatible (ABOi) graft rejection, while donor-specific anti-HLA antibodies and, more recently, autoantibodies are appreciated as important contributors to allograft inflammation and dysfunction. In August 2016, the International Summit of the Canadian National Transplant Research Program focused on recent advances in the field of antibody-mediated rejection. Here, we describe work presented and discussed at the meeting, with a focus on 3 major themes: the importance of 1- Natural antibodies and autoantibodies, 2- tissue injury derived exosomes and autoimmunity, 3- inflammasome activation and innate immune responses in regulating allograft inflammation and dysfunction. Finally, we explore novel areas of therapeutic intervention that have recently emerged from these 3 major and overlapping fields of transplantation research.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

Autoantibodies Against PFDN2 Are Associated With An Increased Risk of Type 2 Diabetes: A Case-Control Study.

The adaptive immune system is involved in type 2 diabetes mellitus (T2DM), indicating the presence of unidentified autoantibodies that might be useful biomarkers for emerging immunomodulatory therapy. A prior microarray study with a small number of participants suggested the association of novel autoantibodies with T2DM in Southwest American Indians (SAIs). We therefore sought to determine whether antibodies against 14 target proteins are associated with T2DM in a large case-control study.

Crypt hyperplastic enteropathy in distal duodenum in Helicobacter pylori infection - report of two cases without evidence of celiac disease.

Patients with Helicobacter pylori (HP) infection have been reported to have in addition to duodenitis architectural changes of the duodenal bulb mucosa including villous atrophy and crypt hyperplasia. We here for the first time present two cases of HP-infected adult patients with a crypt hyperplastic enteropathy also in the distal duodenum mimicking celiac disease (CD).

Exposure to the Epstein-Barr Viral Antigen Latent Membrane Protein 1 Induces Myelin-Reactive Antibodies In Vivo.

Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease of the central nervous system (CNS). Cross-reactivity of neuronal proteins with exogenous antigens is considered one of the possible mechanisms of MS triggering. Previously, we showed that monoclonal myelin basic protein (MBP)-specific antibodies from MS patients cross-react with Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1). In this study, we report that exposure of mice to LMP1 results in induction of myelin-reactive autoantibodies in vivo. We posit that chronic exposure or multiple acute exposures to viral antigen may redirect B cells from production of antiviral antibodies to antibodies, specific to myelin antigen. However, even in inbred animals, which are almost identical in terms of their genomes, such an effect is only observed in 20-50% of animals, indicating that this change occurs by chance, rather than systematically. Cross-immunoprecipitation analysis showed that only part of anti-MBP antibodies from LMP1-immunized mice might simultaneously bind LMP1. In contrast, the majority of anti-LMP1 antibodies from MBP-immunized mice bind MBP. De novo sequencing of anti-LMP1 and anti-MBP antibodies by mass spectrometry demonstrated enhanced clonal diversity in LMP1-immunized mice in comparison with MBP-immunized mice. We suggest that induction of MBP-reactive antibodies in LMP1-immunized mice may be caused by either Follicular dendritic cells (FDCs) or by T cells that are primed by myelin antigens directly in CNS. Our findings help to elucidate the still enigmatic link between EBV infection and MS development, suggesting that myelin-reactive antibodies raised as a response toward EBV protein LMP1 are not truly cross-reactive but are primarily caused by epitope spreading.

Associations of Autoimmunity, Immunodeficiency, Lymphomagenesis, and Gut Microbiota in Mice with Knockins for a Pathogenic Autoantibody.

A number of mouse strains transgenic for B-cell receptors specific for nucleic acids or other autoantigens have been generated to understand how autoreactive B cells are regulated in normal and autoimmune mice. Previous studies of nonautoimmune C57BL/6 mice heterozygous for both the IgH and IgL knockins of the polyreactive autoantibody, 564, produced high levels of autoantibodies in a largely Toll-like receptor 7-dependent manner. Herein, we describe studies of mice homozygous for the knockins that also expressed high levels of autoantibodies but, unlike the heterozygotes, exhibited a high incidence of mature B-cell lymphomas and enhanced susceptibility to bacterial infections. Microarray analyses and serological studies suggested that lymphomagenesis might be related to chronic B-cell activation promoted by IL-21. Strikingly, mice treated continuously with antibiotic-supplemented water did not develop lymphomas or abscesses and exhibited less autoimmunity. This mouse model may help us understand the reasons for enhanced susceptibility to lymphoma development exhibited by humans with a variety of autoimmune diseases, such as Sjögren syndrome, systemic lupus erythematosus, and highly active rheumatoid arthritis.

Single-Session High-Intensity Focused Ultrasound Treatment for Persistent or Relapsed Graves Disease: Preliminary Experience in a Prospective Study.

Purpose To evaluate the safety and efficacy of ultrasonography (US)-guided high-intensity focused ultrasound (HIFU) ablation as a treatment for medically refractory Graves disease (GD). Materials and Methods After ethics approval, a prospective trial (NCT02685514) was performed from November 2015 to February 2016. Thirty patients underwent ablation of the entire right and left thyroid lobes, with areas near the tracheal-esophageal groove and common carotid artery left unablated. Serum thyroid-stimulating hormone (TSH), free T4 (FT4), antithyroid autoantibodies, and TSH receptor (TSHR) antibody levels were evaluated afterward, and US color Doppler, US volumetry, and eye assessment were performed. The primary outcome was the 12-month relapse rate. Relapse referred to hyperthyroidism (FT4 > 23 pmol/L) afterward. Variables associated with relapse were analyzed by using binary logistic regression. Results The technical success rate was 96.7%. The cohort comprised entirely women, with a median age of 38.2 years (interquartile range, 29.5-49.0 years). After 12 months, eight patients (26.7%; 95% confidence interval [CI]: 14.19%, 44.95%) experienced relapse. One patient (3.3%; 95% CI: 0.59%, 16.67%) experienced vocal cord palsy, while two patients (6.7%; 95% CI: 1.85%, 21.33%) experienced Horner syndrome, but none of these conditions were permanent. No changes in gland volume, antithyroid autoantibody levels, and ophthalmic parameters were found at 12-month follow-up. Baseline TSHR was found to have decreased significantly at 6- and 12-month follow-up (P < .001 for both). TSHR antibody (odds ratio [OR] = 1.414; 95% CI: 1.018, 1.965; P = .039) and gland volume (OR = 0.557; 95% CI: 0.353, 0.880; P = .012) were associated with 12-month relapse, with higher antibody levels conferring a higher likelihood and smaller gland volumes conferring a lower likelihood. Conclusion US-guided HIFU of the thyroid may be a safe and efficacious treatment in patients with persistent or relapsed GD. However, further study is warranted before it can become mainstream for this indication. (©) RSNA, 2017 Online supplemental material is available for this article.

ANNALS EXPRESS: Experience with newer central nervous system autoantibodies.

In the last decade, a large number of neuronal cell-surface antibodies have been described which are responsible for a range of neuroimmunological central nervous system disorders. Unlike the paraneoplastic antibodies which target intracellular antigens, these antibodies appear to be pathogenic and hence identification and prompt treatment can make a substantial impact on clinical outcomes of these patients. We review the common antibodies against the ionotropic Glutamate receptors (NMDAR, AMPAR), metabotropic Glutamate receptors (mGluR1 and mGluR5), voltage gated potassium channel-complex proteins (LGI1, CASPR2), and other antibodies targeted against Glycine receptor, Glutamic acid decarboxylase (GAD), Gamma Amino Butyric Acid B (GABAB), Dopamine-2-receptor (D2R) and Dipeptidyl-peptidase-like protein 6 (DPPX).

Autoantibody binding in liquid phase to IL-2 in human sera is not type 1 diabetes specific.

Neuronal Surface Autoantibodies in Neuropsychiatric Disorders: Are There Implications for Depression?

Autoimmune diseases are affecting around 7.6-9.4% of the general population. A number of central nervous system disorders, including encephalitis and severe psychiatric disorders, have been demonstrated to associate with specific neuronal surface autoantibodies (NSAbs). It has become clear that specific autoantibodies targeting neuronal surface antigens and ion channels could cause severe mental disturbances. A number of studies have focused or are currently investigating the presence of autoantibodies in specific mental conditions such as schizophrenia and bipolar disorders. However, less is known about other conditions such as depression. Depression is a psychiatric disorder with complex etiology and pathogenesis. The diagnosis criteria of depression are largely based on symptoms but not on the origin of the disease. The question which arises is whether in a subgroup of patients with depression, the symptoms might be caused by autoantibodies targeting membrane-associated antigens. Here, we describe how autoantibodies targeting membrane proteins and ion channels cause pathological effects. We discuss the physiology of these antigens and their role in relation to depression. Finally, we summarize a number of studies detecting NSAbs with a special focus on cohorts that include depression diagnosis and/or show depressive symptoms.

Myo-inositol and selenium reduce the risk of developing overt hypothyroidism in patients with autoimmune thyroiditis.

The beneficial effects obtained by myo-inositol in association with seleno-methionine in patients affected by subclinical hypothyroidism have been recently demonstrated. Here, we evaluate the immune-modulating effect of myo-inositol in association with seleno-methionine in patients with euthyroid autoimmune thyroiditis (AT).