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Journal articles on the topic 'Anti-immunoglobulin E autoantibodies'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2025

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1

Kawasaki, Eiji. "Anti-Islet Autoantibodies in Type 1 Diabetes." International Journal of Molecular Sciences 24, no. 12 (2023): 10012. http://dx.doi.org/10.3390/ijms241210012.

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Anti-islet autoantibodies serve as key markers in immune-mediated type 1 diabetes (T1D) and slowly progressive T1D (SPIDDM), also known as latent autoimmune diabetes in adults (LADA). Autoantibodies to insulin (IAA), glutamic acid decarboxylase (GADA), tyrosine phosphatase-like protein IA-2 (IA-2A), and zinc transporter 8 (ZnT8A) are currently employed in the diagnosis, pathological analysis, and prediction of T1D. GADA can also be detected in non-diabetic patients with autoimmune diseases other than T1D and may not necessarily reflect insulitis. Conversely, IA-2A and ZnT8A serve as surrogate

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2

MORITA, Kazumasa, Akihiro FUJISAWA, Yosuke YAGI, et al. "Immunoglobulin A anti-BP230 autoantibodies in linear immunoglobulin A/immunoglobulin G bullous dermatosis." Journal of Dermatology 38, no. 10 (2011): 1030–32. http://dx.doi.org/10.1111/j.1346-8138.2010.01158.x.

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3

von Gunten, Stephan, Monique Vogel, Alexander Schaub, et al. "Intravenous immunoglobulin preparations contain anti–Siglec-8 autoantibodies." Journal of Allergy and Clinical Immunology 119, no. 4 (2007): 1005–11. http://dx.doi.org/10.1016/j.jaci.2007.01.023.

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4

Di Mario, Umberto, Riccardo Perfetti, Emanuela Anastasi, et al. "Autoantibodies to insulin do appear in non-diabetic patients with autoimmune disorders: Comparison with anti-immunoglobulin antibodies and other autoimmune phenomena." Acta Endocrinologica 122, no. 2 (1990): 303–8. http://dx.doi.org/10.1530/acta.0.1220303.

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Abstract Insulin- and anti-immunoglobulin-antibodies have been recently reported in pre-diabetic subjects: the former has been proposed as a predictive marker of Type I diabetes in non-diabetic-subjects. To evaluate the diabetes-related specificity of these antibodies, the presence of insulin autoantibodies, using a recently developed and highly sensitive competitive radioimmune assay, and of anti-immunoglobulin antibodies together with that of immune complexes and of other autoantibodies has been investigated in patients with organ- or non-organ-specific autoimmune diseases. One hundred and e

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5

Dietrich, G., M. Algiman, Y. Sultan, UE Nydegger, and MD Kazatchkine. "Origin of anti-idiotypic activity against anti-factor VIII autoantibodies in pools of normal human immunoglobulin G (IVIg)." Blood 79, no. 11 (1992): 2946–51. http://dx.doi.org/10.1182/blood.v79.11.2946.2946.

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Abstract Therapeutic preparations of polyspecific IgG obtained from plasma pools of a large number of normal donors (IVIg) express anti-idiotypic activity against a wide spectrum of natural and disease-associated autoantibodies. The present study investigated the origin of anti- idiotypic activity against autoantibodies to factor VIII. The neutralizing activity of pools of IgG against patients' anti-factor VIII autoantibodies was not influenced by the presence of individuals with natural anti-factor VIII antibodies among donors contributing to the pool. A higher frequency of neutralizing antib

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6

Dietrich, G., M. Algiman, Y. Sultan, UE Nydegger, and MD Kazatchkine. "Origin of anti-idiotypic activity against anti-factor VIII autoantibodies in pools of normal human immunoglobulin G (IVIg)." Blood 79, no. 11 (1992): 2946–51. http://dx.doi.org/10.1182/blood.v79.11.2946.bloodjournal79112946.

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Therapeutic preparations of polyspecific IgG obtained from plasma pools of a large number of normal donors (IVIg) express anti-idiotypic activity against a wide spectrum of natural and disease-associated autoantibodies. The present study investigated the origin of anti- idiotypic activity against autoantibodies to factor VIII. The neutralizing activity of pools of IgG against patients' anti-factor VIII autoantibodies was not influenced by the presence of individuals with natural anti-factor VIII antibodies among donors contributing to the pool. A higher frequency of neutralizing antibodies aga

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Hattori, Naoki, Katsuji Ikekubo, Yasuhisa Nakaya, Kaori Kitagawa, and Chiyoko Inagaki. "Immunoglobulin G Subclasses and Prolactin (PRL) Isoforms in Macroprolactinemia Due to Anti-PRL Autoantibodies." Journal of Clinical Endocrinology & Metabolism 90, no. 5 (2005): 3036–44. http://dx.doi.org/10.1210/jc.2004-1600.

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Although macroprolactinemia due to antiprolactin (anti-PRL) autoantibodies is not uncommon among hyperprolactinemic patients, the pathogenesis of such macroprolactinemia is still unknown. We examined IgG subclasses of anti-PRL autoantibodies by enzyme immunoassay, and PRL phosphorylation and isoforms by Western blotting, mass spectrometry, and two-dimensional electrophoresis in six patients with anti-PRL autoantibodies and in 29 controls. PRL-specific IgG subclasses in patients with anti-PRL autoantibodies were heterogeneous, but five of six patients showed IgG4 predominance, which is known to

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8

Senécal, Jean-Luc, Sabrina Hoa, Roger Yang, and Martial Koenig. "Pathogenic roles of autoantibodies in systemic sclerosis: Current understandings in pathogenesis." Journal of Scleroderma and Related Disorders 5, no. 2 (2019): 103–29. http://dx.doi.org/10.1177/2397198319870667.

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The potential pathogenic role for autoantibodies in systemic sclerosis has captivated researchers for the past 40 years. This review answers the question whether there is yet sufficient knowledge to conclude that certain serum autoantibodies associated with systemic sclerosis contribute to its pathogenesis. Definitions for pathogenic, pathogenetic and functional autoantibodies are formulated, and the need to differentiate these autoantibodies from natural autoantibodies is emphasized. In addition, seven criteria for the identification of pathogenic autoantibodies are proposed. Experimental evi

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de Carvalho, Jozélio Freire, Yaniv Sherer, and Yehuda Shoenfeld. "The fine-tuning of anti-oxidized low-density lipoprotein antibodies in cardiovascular disease and thrombosis." Thrombosis and Haemostasis 98, no. 12 (2007): 1157–59. http://dx.doi.org/10.1160/th07-11-0652.

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SummaryAnti-oxidised low-density lipoprotein (anti-oxLDL) antibodies are a heterogeneous group of autoantibodies including both pathogenic and protective subsets. Whereas in most studies the levels of anti-oxLDL antibodies were associated with enhanced atherosclerosis as evaluated by different methods, immunization with oxLDL leads to elevated levels of anti-oxLDL and protection against atherosclerosis. Anti-oxLDL can also be used for immunomodulation of atherosclerosis (i.e. possible therapeutic use of intravenous immunoglobulin, oral tolerance). More specific autoantibodies out of total anti

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10

Sui, Jingzhe, Haiwei Li, Yanqiong Liu, et al. "Correlation study between clinical phenotypes and autoantibodies in systemic sclerosis in Southwest China." Medicine 104, no. 23 (2025): e42639. https://doi.org/10.1097/md.0000000000042639.

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This study investigates the characteristics of baseline data and the correlation between autoantibodies and clinical phenotypes in patients with systemic sclerosis (SSc) from Southwest China. A total of 346 patients diagnosed with SSc between 2021 and 2023 were included. Clinical data and laboratory data were collected to analyze the relationship between autoantibodies and clinical phenotypes. The prevalence of hypertension and osteoporosis in female patients with SSc was significantly higher than that in male patients. Anti-Scl-70 antibody was positively correlated with Raynaud phenomenon, fa

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11

Terness, P., and G. Opelz. "Natural Anti-Immunoglobulin Autoantibodies: Irrelevant By-Products or Immunoregulatory Molecules?" International Archives of Allergy and Immunology 115, no. 4 (1998): 270–77. http://dx.doi.org/10.1159/000069457.

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12

Halpern, M. D., S. Y. Craven, P. L. Cohen, and R. A. Eisenberg. "Regulation of anti-Sm autoantibodies by the immunoglobulin heavy chain locus." Journal of Immunology 151, no. 12 (1993): 7268–72. http://dx.doi.org/10.4049/jimmunol.151.12.7268.

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Abstract Anti-Sm antibodies are specific markers for systemic lupus erythematosus in MRL mice and in humans. The prevalence of anti-Sm positivity in inbred MRL/Mp-lpr/lpr(MRL/lpr) mice is consistently about 25% at 5 mo of age, when the disease is at its peak. The control of the development of anti-Sm in individual MRL/lpr mice has been shown to be the result of stochastic factors, and previous research has indicated that the immunoglobulin heavy chain (IgH) b allotype may be more amenable to the production of anti-Sm. We have now further investigated the influence of the IgH genetic locus on t

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13

Galeotti, Caroline, Anupama Karnam, Mrinmoy Das, Srini V. Kaveri та Jagadeesh Bayry. "Acid Stripping of Surface IgE Antibodies Bound to FcεRI Is Unsuitable for the Functional Assays That Require Long-Term Culture of Basophils and Entire Removal of Surface IgE". International Journal of Molecular Sciences 21, № 2 (2020): 510. http://dx.doi.org/10.3390/ijms21020510.

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Basophils are rare granulocytes and dysregulated functions of these cells are associated with several atopic and non-atopic allergic diseases of skin, respiratory system and gastrointestinal tract. Both cytokines and immunoglobulin E (IgE) are implicated in mediating the basophil activation and pathogenesis of these disorders. Several reports have shown that healthy individuals, and patients with allergic disorders display IgG autoantibodies to IgE and hence functional characterization of these anti-IgE IgG autoantibodies is critical. In general, anti-IgE IgG autoantibodies modulate basophil a

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14

Sugenoya, Akira, Emiko Mizuno, Masayuki Haniuda, et al. "Anti-triiodothyronine autoantibodies in a euthyroid woman: Confirmation of immunoglobulin G antibodies employing protein A column chromatography." Acta Endocrinologica 124, no. 1 (1991): 115–20. http://dx.doi.org/10.1530/acta.0.1240115.

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Abstract. The presence of thyroid hormone autoantibodies was investigated in a 48-year-old non-goitrous woman with high levels of serum total T3 and free T3. Her other thyroid function tests were normal. The presence of thyroid hormone autoantibodies were assessed in serum, acid-charcoal treated serum, IgG fractions and in a purified IgG fraction. The IgG fraction was separated from serum by a protein A-Sepharose CL-4B column chromatography and purified by gel filtration chromatography using Sephacryl S 200. Sera from normal individuals were used as controls. The results showed that the increa

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15

Tiede, Andreas, Christoph J. Hofbauer, Sonja Werwitzke, et al. "Anti–factor VIII IgA as a potential marker of poor prognosis in acquired hemophilia A: results from the GTH-AH 01/2010 study." Blood 127, no. 19 (2016): 2289–97. http://dx.doi.org/10.1182/blood-2015-09-672774.

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Key Points This study is the first to assess the prognostic value of FVIII-specific antibody data in patients with AHA. Anti-FVIII IgA, but not immunoglobulin G, autoantibodies at baseline are potential predictors of recurrence and poor outcome of AHA.

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16

Hattori, Naoki, Katsuji Ikekubo, Takashi Ishihara, Kunisaburo Moridera, Megumu Hino, and Hiroyuki Kurahachi. "Effects of anti-prolactin autoantibodies on serum prolactin measurements." European Journal of Endocrinology 130, no. 5 (1994): 434–37. http://dx.doi.org/10.1530/eje.0.1300434.

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Hattori N, Ikekubo K, Ishihara T, Moridera K, Hino M, Kurahachi H. Effects of anti-prolactin autoantibodies on serum prolactin measurements. Eur J Endocrinol 1994:130:434–7. ISSN 0804–4643 The influence of anti-PRL autoantibodies on PRL measurements determined by immunoassays was investigated in 10 patients with anti-PRL autoantibodies. Four different immunoassay systems (two double-antibody radioimmunoassays (RIAs), a single-antibody RIA and an immunoradiometric assay (IRMA)) were examined. Total and free PRL were extracted from sera by precipitating γ-globulin with polyethylene glycol with a

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17

Sellebjerg, Finn, Michael Christiansen, and Peter Garred. "MBP, anti-MBP and anti-PLP antibodies, and intrathecal complement activation in multiple sclerosis." Multiple Sclerosis Journal 4, no. 3 (1998): 127–31. http://dx.doi.org/10.1177/135245859800400307.

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Intrathecal immunoglobulin synthesis and activation of the complement cascade occurs in patients with multiple sclerosis (MS). The present study aimed at further studying the relation between intrathecal immunoglobulin synthesis and complement activation. We compared total intrathecal synthesis of lgA, IgG, and IgM, the number of cells secreting anti-myelin basic protein (MBP) and anti-proteolipid protein (PLP) antibodies of the IgG isotype and intrathecal activation of the complement cascade in patients with possible onset symptoms of MS (n=18) or clinically definite MS (n=30). Early activati

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18

Tabata, Nobutada, Masaaki Miyazawa, Ryuichi Fujisawa, Yumiko A. Takei, Hiroyuki Abe, and Keiji Hashimoto. "Establishment of Monoclonal Anti-Retroviral gp70 Autoantibodies from MRL/lpr Lupus Mice and Induction of Glomerular gp70 Deposition and Pathology by Transfer into Non-Autoimmune Mice." Journal of Virology 74, no. 9 (2000): 4116–26. http://dx.doi.org/10.1128/jvi.74.9.4116-4126.2000.

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ABSTRACT Several strains of mice, including MRL/MpJ mice homozygous for the Fas mutant lpr gene (MRL/lpr mice), F1 hybrids of New Zealand Black and New Zealand White mice, and BXSB/MpJ mice carrying a Y-linked autoimmune acceleration gene, spontaneously develop immune complex-mediated glomerulonephritis. The involvement of the envelope glycoprotein gp70 of an endogenous xenotropic virus in the formation of circulating immune complexes and their deposition in the glomerular lesions have been demonstrated, as has the pathogenicity of various antinuclear, antiphospholipid, and rheumatoid factor a

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Frontzek, Karl, Manfredi Carta, Marco Losa, et al. "Autoantibodies against the prion protein in individuals with PRNP mutations." Neurology 95, no. 14 (2020): e2028-e2037. http://dx.doi.org/10.1212/wnl.0000000000009183.

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ObjectiveTo determine whether naturally occurring autoantibodies against the prion protein are present in individuals with genetic prion disease mutations and controls, and if so, whether they are protective against prion disease.MethodsIn this case–control study, we collected 124 blood samples from individuals with a variety of pathogenic PRNP mutations and 78 control individuals with a positive family history of genetic prion disease but lacking disease-associated PRNP mutations. Antibody reactivity was measured using an indirect ELISA for the detection of human immunoglobulin G1–4 antibodie

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Sakakibara, Shuhei, Yu-Chen Liu, Masakazu Ishikawa, et al. "Clonal landscape of autoantibody-secreting plasmablasts in COVID-19 patients." Life Science Alliance 7, no. 12 (2024): e202402774. http://dx.doi.org/10.26508/lsa.202402774.

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Whereas severe COVID-19 is often associated with elevated autoantibody titers, the underlying mechanism behind their generation has remained unclear. Here we report clonal composition and diversity of autoantibodies in humoral response to SARS-CoV-2. Immunoglobulin repertoire analysis and characterization of plasmablast-derived monoclonal antibodies uncovered clonal expansion of plasmablasts producing cardiolipin (CL)-reactive autoantibodies. Half of the expanded CL-reactive clones exhibited strong binding to SARS-CoV-2 antigens. One such clone, CoV1804, was reactive to both CL and viral nucle

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Vogel, Monique, and Paul Engeroff. "A Comparison of Natural and Therapeutic Anti-IgE Antibodies." Antibodies 13, no. 3 (2024): 58. http://dx.doi.org/10.3390/antib13030058.

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Immunoglobulin E (IgE) plays a critical role for the immune system, fighting against parasites, toxins, and cancer. However, when it reacts to allergens without proper regulation, it can cause allergic reactions, including anaphylaxis, through a process initiated by effector cells such as basophils and mast cells. These cells display IgE on their surface, bound to the high-affinity IgE receptor FcεRI. A cross-linking antigen then triggers degranulation and the release of inflammatory mediators from the cells. Therapeutic monoclonal anti-IgE antibodies such as omalizumab, disrupt this process a

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O’Neil, Liam J., Ana Barrera-Vargas, Donavon Sandoval-Heglund, et al. "Neutrophil-mediated carbamylation promotes articular damage in rheumatoid arthritis." Science Advances 6, no. 44 (2020): eabd2688. http://dx.doi.org/10.1126/sciadv.abd2688.

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Formation of autoantibodies to carbamylated proteins (anti-CarP) is considered detrimental in the prognosis of erosive rheumatoid arthritis (RA). The source of carbamylated antigens and the mechanisms by which anti-CarP antibodies promote bone erosion in RA remain unknown. Here, we find that neutrophil extracellular traps (NETs) externalize carbamylated proteins and that RA subjects develop autoantibodies against carbamylated NET (cNET) antigens that, in turn, correlate with levels of anti-CarP. Transgenic mice expressing the human RA shared epitope (HLADRB1* 04:01) immunized with cNETs develo

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Lei, Meng-Huan, Po-Wen Hsu, Yin-Tai Tsai, et al. "Low Levels of IgM Recognizing 4-Hydroxy-2-Nonenal-Modified Apolipoprotein A-I Peptide and Its Association with the Severity of Coronary Artery Disease in Taiwanese Patients." Current Issues in Molecular Biology 46, no. 6 (2024): 6267–83. http://dx.doi.org/10.3390/cimb46060374.

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Autoantibodies against apolipoprotein A-I (ApoA-I) are associated with cardiovascular disease risks. We aimed to examine the 4-hydroxy-2-nonenal (HNE) modification of ApoA-I in coronary artery disease (CAD) and evaluate the potential risk of autoantibodies against their unmodified and HNE-modified peptides. We assessed plasma levels of ApoA-I, HNE-protein adducts, and autoantibodies against unmodified and HNE-peptide adducts, and significant correlations and odds ratios (ORs) were examined. Two novel CAD-specific HNE-peptide adducts, ApoA-I251–262 and ApoA-I70–83, were identified. Notably, imm

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Roose, Elien, Gestur Vidarsson, Kadri Kangro, et al. "Anti-ADAMTS13 Autoantibodies against Cryptic Epitopes in Immune-Mediated Thrombotic Thrombocytopenic Purpura." Thrombosis and Haemostasis 118, no. 10 (2018): 1729–42. http://dx.doi.org/10.1055/s-0038-1669459.

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AbstractImmune-mediated thrombotic thrombocytopenic purpura (iTTP) is characterized by severe ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13) deficiency, the presence of anti-ADAMTS13 autoantibodies and an open ADAMTS13 conformation with a cryptic epitope in the spacer domain exposed. A detailed knowledge of anti-ADAMTS13 autoantibodies will help identifying pathogenic antibodies and elucidating the cause of ADAMTS13 deficiency. We aimed at cloning anti-ADAMTS13 autoantibodies from iTTP patients to study their epitopes and inhibitory characteristics.

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Bierła, Joanna B., Bożena Cukrowska, Barbara Skrzydło-Radomańska, et al. "The Occurrence of Gluten-Related Antibodies, Sensitization to Selected Food Allergens, and Antibodies against Intrinsic Factor in Adult Patients with Diarrhea-Predominant Irritable Bowel Syndrome." Journal of Personalized Medicine 13, no. 7 (2023): 1165. http://dx.doi.org/10.3390/jpm13071165.

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Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder. Due to the possible overlap of IBS clinical symptoms with gluten-related diseases, food allergies, and autoimmune gastritis (AIG), the aim of this study was to present the frequency of anti-tissue transglutaminase 2 (TTG2) autoantibodies, anti-deamidated gluten peptide (DGP) antibodies, specific immunoglobulin E antibodies (sIgE) to selected food allergens, and anti-intrinsic factor (IF) autoantibodies in adult patients with diarrhea-predominant IBS (IBS-D). The study involved 244 patients (170 women) aged 18–75 y

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von Gunten, Stephan, Alexander Schaub, Monique Vogel, Beda M. Stadler, Sylvia Miescher, and Hans-Uwe Simon. "Immunologic and functional evidence for anti–Siglec-9 autoantibodies in intravenous immunoglobulin preparations." Blood 108, no. 13 (2006): 4255–59. http://dx.doi.org/10.1182/blood-2006-05-021568.

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Abstract Human intravenous immunoglobulin (IVIg) preparations are increasingly used for the treatment of autoimmune diseases. Earlier work demonstrated the presence of autoantibodies against Fas in IVIg, suggesting that IVIg might be able to induce caspase-dependent cell death in Fas-sensitive cells. In this study, we demonstrate that sialic acid–binding Ig-like lectin 9 (Siglec) represents a surface molecule on neutrophils that is activated by IVIg, resulting in caspase-dependent and caspase-independent forms of cell death. Neutrophil death was mediated by naturally occurring anti–Siglec-9 au

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Hennig, C., L. Rink, and H. Kirchner. "Evidence for presence of lgG4 anti-immunoglobulin autoantibodies in all human beings." Lancet 355, no. 9215 (2000): 1617–18. http://dx.doi.org/10.1016/s0140-6736(00)02223-6.

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Plaimauer, Barbara, Silvia Ferrari, Bernadette Gruber, et al. "Detection of Circulating ADAMTS13 Immune Complexes by Antibody Class-Specific ELISA." Blood 118, no. 21 (2011): 4361. http://dx.doi.org/10.1182/blood.v118.21.4361.4361.

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Abstract Abstract 4361 A severe functional deficiency of the von Willebrand factor (VWF) cleaving protease ADAMTS13 results in the accumulation of uncleaved, highly adhesive VWF multimers in plasma leading to increased platelet aggregation and thrombus formation in the microcirculation. Anti-ADAMTS13 autoantibodies that either neutralize ADAMT13’s activity or enhance protein clearance are the major cause of severe ADAMTS13 deficiency in acquired thrombotic thrombocytopenic purpura (TTP). Circulating anti-ADAMTS13 immune complexes that may play a role in disease pathogenesis have been described

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Baek, Han-Sang, and Dong-Jun Lim. "Interpretation of Thyroid Autoantibodies in Hyperthyroidism." Korean Journal of Medicine 98, no. 3 (2023): 132–36. http://dx.doi.org/10.3904/kjm.2023.98.3.132.

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Thyrotoxicosis is a clinical state with a variety of various etiologies that results from excess thyroid hormones, including hyperthyroidism and thyroiditis. Graves' disease (GD) is a well-known autoimmune thyroid disease that causes hyperthyroidism, and its pathogenesis is mainly driven by the thyroid-stimulating hormone receptor antibody (TSHRAb), which is highly specific for GD. Measuring the TSHRAb is a fast and accurate diagnostic tool for GD and has been used to monitor disease activity and the treatment response. However, conventional TSH-binding inhibitory immunoglobulin (TBII) does no

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van Es, J. H., F. H. Gmelig Meyling, W. R. van de Akker, H. Aanstoot, R. H. Derksen, and T. Logtenberg. "Somatic mutations in the variable regions of a human IgG anti-double-stranded DNA autoantibody suggest a role for antigen in the induction of systemic lupus erythematosus." Journal of Experimental Medicine 173, no. 2 (1991): 461–70. http://dx.doi.org/10.1084/jem.173.2.461.

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The processes that govern the generation of pathogenic anti-DNA autoantibodies in human systemic lupus erythematosus (SLE) are largely unknown. Autoantibodies may arise as a consequence of polyclonal B cell activation and/or antigen-driven B cell activation and selection. The role of these processes in humoral autoimmunity may be studied by molecular genetic analysis of immunoglobulin (Ig) variable (V) regions of antibodies that are characteristic of SLE. We have analyzed the gene elements that encode a high affinity, IgG anti-double-stranded DNA autoantibody secreted by a monoclonal Epstein-B

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Kozyr, A. V., A. V. Kolesnikov, A. E. Khlyntseva, et al. "Role of Structure-Based Changes due to Somatic Mutation in Highly Homologous DNA-Binding and DNA-Hydrolyzing Autoantibodies Exemplified by A23P Substitution in the VH Domain." Autoimmune Diseases 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/683829.

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Anti-DNA autoantibodies are responsible for tissue injury in lupus. A subset of DNA-specific antibodies capable of DNA cleavage can be even more harmful after entering the living cells by destroying nuclear DNA. Origins of anti-DNA autoantibodies are not fully understood, and the mechanism of induction of DNA-cleaving activity remains speculative. The autoantibody BV04-01 derived from lupus-prone mouse is the only DNA-hydrolyzing immunoglobulin with known 3D structure. Identification and analysis of antibodies homologous to BV04-01 may help to understand molecular bases and origins of DNA-clea

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Kole, Hemanta, Bethany Scott та Silvia Bolland. "Understanding lupus pathology in FcγRIIB-/-yaa mice: autoantibodies and autoantigens (P4008)". Journal of Immunology 190, № 1_Supplement (2013): 42.5. http://dx.doi.org/10.4049/jimmunol.190.supp.42.5.

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Abstract FcγRIIB knock-out mice in B6 background develop a lupus like autoimmune disease. With the addition of the yaa (Y-chromosome autoimmune accelerator) gene, pathogenecity in these male mice is significantly enhanced and autoantibodies switch from nuclear to nucleolar specificity. High titer of λ-light chains immunoglobulin, and anti-RNA antibodies were found in R2-/-yaa serum. Also, R2-/-yaa serum selectively bound 5 major nuclear proteins compared to R2-/- serum. To characterize the autoantibodies produced by R2-/-yaa mice and the nucleolar antigens that react with these antibodies, we

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Hansson, Tony, Ingrid Dahlbom, Siv Rogberg, et al. "Antitissue Transglutaminase and Antithyroid Autoantibodies in Children with Down Syndrome and Celiac Disease." Journal of Pediatric Gastroenterology and Nutrition 40, no. 2 (2005): 170–74. http://dx.doi.org/10.1002/j.1536-4801.2005.tb00958.x.

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ABSTRACTObjectives:We measured circulating autoantibodies and evaluated the potential of circulating antitissue transglutaminase (tTG) antibodies to determine the presence of celiac disease (CD) in children with Down syndrome.Methods:An ELISA based on recombinant human tTG was used to measure the levels of immunoglobulin A and immunoglobulin G antibodies in serum samples from 72 children with Down syndrome, 52 children with biopsy‐verified CD, 21 disease controls with a normal small intestinal mucosa and 23 healthy controls. Of the 72 Down syndrome children, 11 under‐went a small intestinal bi

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Yang, L. J., H. G. Li, A. Q. Zeng, et al. "AB0296 PASSIVE TRANSFER OF ANTI-SSA, ANTI-Ro52, AND ANTI-MITOCHONDRIAL M2 FROM INTRAVENOUS IMMUNOGLOBULIN PRODUCTS TO PATIENTS WITH RHEUMATIC DISEASES." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 1174.2–1174. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3544.

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Background:Passive transfer of ANA and anti-SSA has been reported in patients with common variable immunodeficiency disorder who received intravenous immunoglobulin (IVIG). IVIG is also recommended to treat some special or life-threatening rheumatic diseases.Objectives:This study was aimed to explore whether any extractable nuclear antibodies (ENAs) were transferred to these rheumatic patients who received IVIG therapy.Methods:IVIG products of three batches were tested for ANA by using indirect immunofluorescent assay, and for ENAs by using line immunoassay (LIA) and chemiluminescence immunoas

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Sun, RS, XH Chen, JF Sui та ін. "Detecting Anti-FcεRI Autoantibodies in Patients with Asthma by Flow Cytometry". Journal of International Medical Research 36, № 6 (2008): 1214–19. http://dx.doi.org/10.1177/147323000803600607.

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Autoimmune diseases have been implicated in the development of intrinsic asthma, however little data are available on the role of autoimmunity in the pathogenesis of asthma. The purpose of this study was to investigate circulating autoantibodies against the high-affinity receptor for immunoglobulin E, FcεRI, in patients with asthma. Seventy-eight patients with asthma and 32 healthy control subjects were included. All individuals were tested using a triple-staining flow cytometry-based basophil activation test (BAT) for the potential presence of autoantibodies against FcεRI. Of the 78 asthma pa

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Maślińska, Maria, Małgorzata Mańczak, Brygida Kwiatkowska, Vince Ramsperger, Long Shen, and Lakshmanan Suresh. "IgA immunoglobulin isotype of rheumatoid factor in primary Sjögren’s syndrome." Rheumatology International 41, no. 3 (2021): 643–49. http://dx.doi.org/10.1007/s00296-020-04782-3.

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AbstractPrimary Sjögren’s syndrome (pSS) is an autoimmune disease with autoantibodies overproduction, including rheumatoid factors (RF). RF-IgA, IgG immunoglobulin classes are suggested as potential biomarkers of pSS. We studied 76 patients with pSS (ACR/Eular 2017); laboratory tests included ESR, C-reactive protein, concentrations of gamma globulins, RF, Anti-SS-A/Ro, and anti-SS-B/La. Eye dryness and keratoconjunctivitis sicca were confirmed with Schirmer’s test, the ocular staining score (OSS) using lissamine green, fluorescein staining and biopsy of minor salivary gland with the histopatho

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Di Mario, U., L. Crisa, E. Anastasi, et al. "Anti-goat immunoglobulin antibodies in diabetic children at diagnosis and follow-up: comparison with islet cell antibodies and other autoantibodies." Acta Endocrinologica 120, no. 3 (1989): 326–30. http://dx.doi.org/10.1530/acta.0.1200326.

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Abstract. The presence of antibodies reacting with human as well as animal immunoglobulins in sera from recent onset Type I diabetic patients has been recently demonstrated by some of our group. In the present study, the occurrence of these antibodies has been evaluated in sera from 19 Type I diabetic patients, at diagnosis and at follow-up within three years, and from 26 normal subjects, and has also been compared with the presence of islet cell antibodies and other organ-specific autoantibodies. A solid-phase radioimmunoassay has been used: serum was incubated in goat immunoglobulin-coated w

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Ehlers, Marc, Hidehiro Fukuyama, Tracy L. McGaha, Alan Aderem, and Jeffrey V. Ravetch. "TLR9/MyD88 signaling is required for class switching to pathogenic IgG2a and 2b autoantibodies in SLE." Journal of Experimental Medicine 203, no. 3 (2006): 553–61. http://dx.doi.org/10.1084/jem.20052438.

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Loss of tolerance in systemic lupus erythematosus (SLE) leads to the generation of autoantibodies, which accumulate in end-organs where they induce disease. Here we show that immunoglobulin (Ig)G2a and 2b autoantibodies are the pathogenic isotypes by recruiting FcγRIV expressing macrophages. Class switching, but not development, of IgM anti-self B cells to these pathogenic subclasses requires the innate immune receptor Toll-like receptor (TLR)9 and MyD88 signaling. In their absence, switching of autoreactive B cells to the IgG2a and 2b subclasses is blocked, resulting in reduced pathology and

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Eisenberg, Robert, Arpita Choudhury, Eline Luning Prak, and Mark Schlissel. "Secondary light chain gene rearrangements in the generation of anti-DNA autoantibodies in the chronic graft-versus-host model of SLE (44.15)." Journal of Immunology 186, no. 1_Supplement (2011): 44.15. http://dx.doi.org/10.4049/jimmunol.186.supp.44.15.

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Abstract The loss of B-cell tolerance to nuclear autoantigens is central to the pathogenesis of SLE, but it is not known which tolerance checkpoints fail in the production of anti-DNA autoantibodies. We have utilized the chronic GVH model of SLE to target the loss of tolerance to mature, splenic B cells (JI 179, 5564, 2007). We have now extended these studies to show that the production of these autoantibodies involves the switching of κ-chain alleles in mature B cells. We have distinguished the two κ alleles by utilizing a genetic locus in which the human κ constant region has replaced the mo

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Schou, M., S. G. Sæther, K. Borowski, et al. "Prevalence of serum anti-neuronal autoantibodies in patients admitted to acute psychiatric care." Psychological Medicine 46, no. 16 (2016): 3303–13. http://dx.doi.org/10.1017/s0033291716002038.

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BackgroundAutoimmune encephalitis associated with anti-neuronal antibodies may be challenging to distinguish from primary psychiatric disorders. The significance of anti-neuronal antibodies in psychiatric patients without clear evidence of autoimmune encephalitis is unknown. We investigated the serum prevalence of six anti-neuronal autoantibodies in a cohort of unselected patients admitted to acute psychiatric care.MethodSerum was drawn from 925 patients admitted to acute psychiatric in-patient care. Psychiatric diagnoses were set according to International Classification of Diseases (ICD)-10

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Berchtold, P., GL Dale, P. Tani, and R. McMillan. "Inhibition of autoantibody binding to platelet glycoprotein IIb/IIIa by anti-idiotypic antibodies in intravenous gammaglobulin." Blood 74, no. 7 (1989): 2414–17. http://dx.doi.org/10.1182/blood.v74.7.2414.2414.

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Abstract Intravenous immunoglobulin (IVIgG) causes an acute rise in the platelet count in the majority of patients with chronic immune thrombocytopenic purpura (ITP) but the mechanism(s) of action is still unknown. We evaluated the ability of three different IVIgG preparations to inhibit the in vitro binding of autoantibody to platelet glycoprotein (GP) IIb/IIIa. ITP plasma, known to contain anti-GPIIb/IIIa antibodies, was incubated overnight with either IVIgG or bovine serum albumin (BSA) followed by measurement of the autoantibody titer. Binding of autoantibody from eight ITP patients was in

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Berchtold, P., GL Dale, P. Tani, and R. McMillan. "Inhibition of autoantibody binding to platelet glycoprotein IIb/IIIa by anti-idiotypic antibodies in intravenous gammaglobulin." Blood 74, no. 7 (1989): 2414–17. http://dx.doi.org/10.1182/blood.v74.7.2414.bloodjournal7472414.

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Intravenous immunoglobulin (IVIgG) causes an acute rise in the platelet count in the majority of patients with chronic immune thrombocytopenic purpura (ITP) but the mechanism(s) of action is still unknown. We evaluated the ability of three different IVIgG preparations to inhibit the in vitro binding of autoantibody to platelet glycoprotein (GP) IIb/IIIa. ITP plasma, known to contain anti-GPIIb/IIIa antibodies, was incubated overnight with either IVIgG or bovine serum albumin (BSA) followed by measurement of the autoantibody titer. Binding of autoantibody from eight ITP patients was inhibited b

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Yamagami, Jun. "Recent advances in the understanding and treatment of pemphigus and pemphigoid." F1000Research 7 (August 30, 2018): 1360. http://dx.doi.org/10.12688/f1000research.14474.1.

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Pemphigus and pemphigoid are characterized as autoimmune blistering diseases in which immunoglobulin G autoantibodies cause blisters and erosions of the skin or mucosa or both. Recently, understanding of the pathophysiology of pemphigus and pemphigoid has been furthered by genetic analyses, characterization of autoantibodies and autoreactive B cells, and elucidation of cell–cell adhesion between keratinocytes. For the management of pemphigus and pemphigoid, the administration of systemic corticosteroids still represents the standard treatment strategy; however, evidence of the efficacy of ther

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Pott, Marian-Christopher, Natalie Frede, Jennifer Wanders, et al. "Autoantibodies against BAFF, APRIL or IL21 - an alternative pathogenesis for antibody-deficiencies?" BMC Immunology 18, no. 1 (2017): 34. https://doi.org/10.1186/s12865-017-0217-9.

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<strong>Background: </strong>The ability of anti-cytokine antibodies to play a disease-causing role in the pathogenesis of immunodeficiencies is widely accepted. The aim of this study was to investigate whether autoantibodies against BAFF (important B cell survival signal), APRIL (important plasma cell survival signal), or Interleukin-21 (important cytokine for immunoglobulin class switch) present an alternative mechanism for the development of the following primary antibody deficiencies (PADs): common variable immune deficiency (CVID) or selective IgA deficiency (sIgAD).<strong>Results: </str

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Cuchacovich, Miguel, Héctor Gatica, Paula Vial, Jorge Yovanovich, Salvatore V. Pizzo, and Mario Gonzalez-Gronow. "Streptokinase Promotes Development of Dipeptidyl Peptidase IV (CD26) Autoantibodies after Fibrinolytic Therapy in Myocardial Infarction Patients." Clinical and Vaccine Immunology 9, no. 6 (2002): 1253–59. http://dx.doi.org/10.1128/cdli.9.6.1253-1259.2002.

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ABSTRACT Dipeptidyl peptidase IV (DPP IV) (CD26) plays a critical role in the modulation and expression of autoimmune and inflammatory diseases. We recently reported that sera from patients with rheumatoid arthritis and systemic lupus erythematosus contained low levels of DPP IV and high titers of anti-DPP IV autoantibodies of the immunoglobulin A (IgA) and IgG classes and found a correlation between the low circulating levels of DPP IV and the high titers of anti-DPP IV autoantibodies of the IgA class. Since streptokinase (SK) is a potent immunogen and binds to DPP IV, we speculated that pati

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KOTANI, TOMIO, EIICHI KATO, KEISUKE HIRAI, KANJI KUMA, and SACHIYA OHTAKI. "Immunoglobulin G subclasses of anti-thyroid peroxidase autoantibodies in human autoimmune thyroid diseases." Endocrinologia Japonica 33, no. 4 (1986): 505–10. http://dx.doi.org/10.1507/endocrj1954.33.505.

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Lee, Lela A., Silvija Coulter, Susan Erner, and Henry Chu. "Cardiac immunoglobulin deposition in congenital heart block associated with maternal anti-Ro autoantibodies." American Journal of Medicine 83, no. 4 (1987): 793–96. http://dx.doi.org/10.1016/0002-9343(87)90918-1.

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Morita, Ryoko, Naoki Oiso, Norito Ishii, et al. "Case of burn-associated bullous pemphigoid caused by anti-BP230 immunoglobulin G autoantibodies." Journal of Dermatology 42, no. 6 (2015): 657–58. http://dx.doi.org/10.1111/1346-8138.12848.

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Fairley, Janet A., Chang Ling Fu, and George J. Giudice. "Mapping the Binding Sites of Anti-BP180 Immunoglobulin E Autoantibodies in Bullous Pemphigoid." Journal of Investigative Dermatology 125, no. 3 (2005): 467–72. http://dx.doi.org/10.1111/j.0022-202x.2005.23853.x.

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Gao, Pan, Xiaowu Chen, Yuhao Li, Fangming Li, and Hongya Zhang. "Anti-CASPR2 meningoencephalitis with thickened dura mater induced by various infections: A case report and literature review." Medicine 104, no. 25 (2025): e42873. https://doi.org/10.1097/md.0000000000042873.

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Rationale: With the update of novel autoantibodies and the expansion of the clinical spectrum, our understanding of autoimmune encephalitis (AE) is rapidly evolving. Anti-CASPR2 meningoencephalitis is a relatively rare condition that may be induced by infections. Patient concerns: A young man presented with 3 episodes of meningoencephalitis potentially triggered by possible viral, Salmonella, and severe acute respiratory syndrome coronavirus 2. Neuroimaging revealed a thickening of the cerebral dura mater. Laboratory tests found positive serum CASPR2 antibodies in the third episode. Diagnoses:

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