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Добірка наукової літератури з теми "Autoantigeni"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Autoantigeni"

1

Preuss, Klaus-Dieter, Gerhard Held, Natalie Fadle, Evi Regitz, Maria Kemele, Stephan Stilgenbauer, Andreas Buehler, and Michael Pfreundschuh. "Autoantigenic Targets of B-Cell Receptors (BCR) Derived From Chronic Lymphocytic Leukemias Bind to and Induce Proliferation of Leukemic Cells." Blood 120, no. 21 (November 16, 2012): 2884. http://dx.doi.org/10.1182/blood.v120.21.2884.2884.

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Abstract Abstract 2884 Background Auto-antigenic targets of the B-cell receptor (BCR) derived from malignant cells in chronic lymphocytic leukemia (CLL) might play a role in the pathogenesis of this neoplasm. Patients and Methods In order to identify autoantigenic targets of CLL-derived BCR we screened human tissue-derived protein macroarrays with Fab fragments obtained by papain treatment of CLL cells derived from 50 consecutive cases. Antigens were biochemically and molecularly characterized and recombinantly expressed. Results An autoantigenic target was identified for 12/50 (24%) of the cases, with 3 autoantigens being the target of the BCR from two patients each. CLL-BCR derived from the same stereotype subset recognized the same antigen, but differed epitopes. By flow cytometry using flag-tagged recombinantly expressed autoantigens binding of antigen to the surface of CLL was demonstrated, which was specific for the CLL cells from which the BCR used for the identification of the respective autoantigen was derived. Moreover, binding of the autoantigen to the respective leukemic cells induced specific activation as shown by increased cytoplasmic calcium concentration, induced MYC expression and proliferation of leukemic CLL cells as demonstrated by a proliferation assay (EZ4U). Conclusions Autoantigens are frequent targets of CLL-derived BCR. Their specific binding to and induction of proliferation in respective leukemic cells, which has been demonstrated for the first time, provide the most convincing evidence to date for the long-time hypothesized role of autoantigens in the pathogenesis of chronic lymphocyte leukemia. Supported by Sander-Stiftung (Munich, Germany) Disclosures: No relevant conflicts of interest to declare.
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2

Sármay, Gabriella. "Biologia Futura: Emerging antigen-specific therapies for autoimmune diseases." Biologia Futura 72, no. 1 (February 4, 2021): 15–24. http://dx.doi.org/10.1007/s42977-021-00074-4.

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AbstractAutoimmune diseases are caused by breaking the central and/or peripheral tolerance against self, leading to uncontrolled immune response to autoantigens. The incidences of autoimmune diseases have increased significantly worldwide over the last decades; nearly 5% of the world's population is affected. The current treatments aim to reduce pain and inflammation to prevent organ damage and have a general immunosuppressive effect, but they cannot cure the disease. There is a huge unmet need for autoantigen-specific therapy, without affecting the immune response against pathogens. This goal can be achieved by targeting autoantigen-specific T or B cells and by restoring self-tolerance by inducing tolerogenic antigen-presenting cells (APC) and the development of regulatory T (Treg) cells, for example, by using autoantigenic peptides bound to nanoparticles. Transferring in vitro manipulated autologous tolerogenic APC or autologous autoantigen-specific Treg cells to patients is the promising approach to develop cellular therapeutics. Most recently, chimeric autoantibody receptor T cells have been designed to specifically deplete autoreactive B cells. Limitations of these novel autoantigen-specific therapies will also be discussed.
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Moritz, Christian P., Yannick Tholance, Oda Stoevesandt, Karine Ferraud, Jean-Philippe Camdessanché, and Jean-Christophe Antoine. "CIDP Antibodies Target Junction Proteins and Identify Patient Subgroups." Neurology - Neuroimmunology Neuroinflammation 8, no. 2 (January 6, 2021): e944. http://dx.doi.org/10.1212/nxi.0000000000000944.

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ObjectiveTo discover systemic characteristics in the repertoires of targeted autoantigens in chronic inflammatory demyelinating polyneuropathy (CIDP), we detected the entire autoantigen repertoire of patients and controls and analyzed them systematically.MethodsWe screened 43 human serum samples, of which 22 were from patients with CIDP, 12 from patients with other neuropathies, and 9 from healthy controls via HuProt Human Proteome microarrays testing about 16,000 distinct human bait proteins. Autoantigen repertoires were analyzed via bioinformatical autoantigenomic approaches: principal component analysis, analysis of the repertoire sizes in disease groups and clinical subgroups, and overrepresentation analyses using Gene Ontology and PantherDB.ResultsThe autoantigen repertoires enabled the identification of a subgroup of 10/22 patients with CIDP with a younger age at onset and a higher frequency of mixed motor and sensory CIDP. IV immunoglobulin therapy responders targeted 3 times more autoantigens than nonresponders. No CIDP-specific autoantibody is present in all patients; however, anchoring junction components were significantly targeted by 86.4% of patients with CIDP. There are potential novel CIDP-specific autoantigens such as the myelination- or axo-glial structure–related proteins actin-related protein 2/3 complex subunit 1B, band 4.1-like protein 2, cadherin-15, cytohesin-1, epidermal growth factor receptor, ezrin, and radixin.ConclusionsThe repertoire of targeted autoantigens of patients with CIDP differs in a systematic degree from those of controls. Systematic autoantigenomic approaches can help to understand the disease and to discover novel bioinformatical tools and novel autoantigen panels to improve diagnosis, treatment, prognosis, or patient stratification.
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Fussey, Shelley P. M., Shauna M. West, J. Gordon Lindsay, C. Ian Ragan, Oliver F. W. James, Margaret F. Bassendine, and Stephen J. Yeaman. "Clarification of the identity of the major M2 autoantigen in primary biliary cirrhosis." Clinical Science 80, no. 5 (May 1, 1991): 451–55. http://dx.doi.org/10.1042/cs0800451.

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1. In primary biliary cirrhosis, the major M2 autoantigen, reacting with antimitochondrial antibodies in sera from >90% of patients, has been identified as the E2 component of the pyruvate dehydrogenase complex. However, two recent reports suggest that alternative polypeptides may be major autoantigens. 2. The evidence that a 75 kDa subunit of complex I of the respiratory chain is a major autoantigen (Frostell, Mendel-Hartvig, Nelson, Totterman, Bjorkland & Ragan, Scand. J. Immunol. 1988; 28, 157–65) is refuted. The findings of Frostell et al. can be explained by contamination of complex I with the pyruvate dehydrogenase complex, evidence for which is presented here. 3. Inspection of the partial amino acid sequence of an unidentified mitochondrial autoantigen (Muno, Kominami, Ishii, Usui, Saituku, Sakakibara & Namihisa, Hepatology 1990; 11, 16–23) shows that it is the El β-subunit of the pyruvate dehydrogenase complex, previously identified as a major autoantigen, and not a ‘new’ alternative major autoantigen. 4. These findings substantiate previous work showing that the mitochondrial M2 autoantigens identified so far in primary biliary cirrhosis are all polypeptide components of the pyruvate dehydrogenase complex or the other related 2-oxo acid dehydrogenase complexes.
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Si, Fuchun. "Identification and expression distribution of esophageal carcinoma autoantigens." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e16520-e16520. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16520.

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e16520 Background: To identify the autoantigen protein molecules with autoserum in the tissues from the esophageal carcinoma (EC) patients, analyze autoantigen expression distribution in EC tissues, so as to provide basis for the molecular pathogenesis and clinical medication of EC. Methods: 69 cases of EC patients tissues and serum and 81 cases of healthy people serum were collected, serological proteome analysis (SERPA) was modified with sequential extraction of subcellular protein fractions to identify esophageal oncopathgensis stages autoantigen with autoserum in the tissues from the EC patients. Another 93 cases of EC patients tissue were collected, immunohistochemical and western blot method were used to detect expression distribution of EC autoantigens in esophageal carcinoma tissue, para-carcinoma tissue and normal tissue. Results: Autoantigens CK13, CK16, CaD, ACTG2, tumor rejection antigen (gp96) 1 variant, heat shock protein gp96 precursor were identified, among wihich, CK16, CaD, ACTG2, tumor rejection antigen (gp96)1 variant, heat shock protein gp96 precursor were firstly reported as EC autoantigens. Expression of autoantigens CK16, CaD, ACTG2 were increased in EC carcinoma tissue than para-carcinoma tissue and normal tissue, while CK13 were decreased. Positive expression level of CK16 in normal tissue, para-carcinoma tissue and cancer tissue of EC patients was 0.0076±0.0033, 0.0158±0.0065, 0.0356±0.0165 respectively, CaD was 0.0085±0.0048, 0.0107±0.0056, 0.0177±0.0103 respectively, ACTG2 was 0.0091±0.0039, 0.0136±0.0043, 0.0214±0.0110 respectively, and CK13 was 0.2053±0.0311, 0.1633±0.0280, 0.0412±0.0239 respectively. Conclusions: 6 EC autoantigens were identified, and 5 were first reported. Autoantigens CK13, CK16, CaD and ACTG2 were expressed in EC patients carcinoma tissue, which can be the potential biomarkers of esophageal carcinoma. This study provides new basis for the EC molecular mechanism and development of molecular drugs.
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Pravda, Jay. "Systemic Lupus Erythematosus: Pathogenesis at the Functional Limit of Redox Homeostasis." Oxidative Medicine and Cellular Longevity 2019 (November 26, 2019): 1–11. http://dx.doi.org/10.1155/2019/1651724.

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Systemic lupus erythematosus (SLE) is a disease characterized by the production of autoreactive antibodies and cytokines, which are thought to have a major role in disease activity and progression. Immune system exposure to excessive amounts of autoantigens that are not efficiently removed is reported to play a significant role in the generation of autoantibodies and the pathogenesis of SLE. While several mechanisms of cell death-based autoantigenic exposure and compromised autoantigen removal have been described in relation to disease onset, a significant association with the development of SLE can be attributed to increased apoptosis and impaired phagocytosis of apoptotic cells. Both apoptosis and impaired phagocytosis can be caused by hydrogen peroxide whose cellular production is enhanced by exposure to endogenous hormones or environmental chemicals, which have been implicated in the pathogenesis of SLE. Hydrogen peroxide can cause lymphocyte apoptosis and glutathione depletion, both of which are associated with the severity of SLE. The cellular accumulation of hydrogen peroxide is facilitated by the myriad of stimuli causing increased cellular bioenergetic activity that enhances metabolic production of this toxic oxidizing agent such as emotional stress and infection, which are recognized SLE exacerbating factors. When combined with impaired cellular hydrogen peroxide removal caused by xenobiotics and genetically compromised hydrogen peroxide elimination due to enzymatic polymorphic variation, a mechanism for cellular accumulation of hydrogen peroxide emerges, leading to hydrogen peroxide-induced apoptosis and impaired phagocytosis, enhanced autoantigen exposure, formation of autoantibodies, and development of SLE.
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Tian, Jun, Yaojun Wang, Ming Ding, Yue Zhang, Jiaoni Chi, Tao Wang, Bin Jiao, et al. "The Formation of Melanocyte Apoptotic Bodies in Vitiligo and the Relocation of Vitiligo Autoantigens under Oxidative Stress." Oxidative Medicine and Cellular Longevity 2021 (October 28, 2021): 1–13. http://dx.doi.org/10.1155/2021/7617839.

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Background. Oxidative stress has a vital role in the early stages of vitiligo. Autoantigens released from apoptotic melanocytes (MC) under oxidative stress are involved in the presentation and recognition of antigens. However, the transport of autoantigens to the cell surface and their release to the extracellular environment are still unclear. Apoptotic bodies (ABs) have always been considered as a key source of immunomodulators and autoantigens. Yet, the role of ABs in the immune mechanism of vitiligo is still unknown. Purpose. To explore whether MC’s autoantigens translocate into ABs during oxidative stress-induced apoptosis and study the molecular mechanisms underlying autoantigen migration and AB formation. Methods. PIG3V (an immortalized human vitiligo melanocyte cell line) were treated with H2O2, and ABs were separated. Transmission electron microscopy, flow cytometry, Western blot, mass spectrometry, and other methods were used to determine the relocation of specific antigens in PIG3V cells to ABs. After pretreatment with specific inhibitors (Rho kinase (Y-27632), myosin light chain kinase (MLCK, ML-9), pan-caspase (zVAD-FMK), and JNK (SP600125)), the pathway of autoantigen translocation into ABs and the formation of apoptotic bodies were determined. Results. When treated with 0.8 mM H2O2, ABs were released from these cells. Autoantigens such as tyrosinase-related protein 1 (TYRP-1) and cleavage nuclear membrane antigen Lamin A/C (Asp230) were concentrated in ABs. The expression of autoantigens and the formation of ABs increased in a time- and dose-dependent manner after treatment with H2O2, while the application of specific inhibitors inhibited the formation of apoptotic bodies, i.e., the expression of antigens. Conclusion. Vitiligo autoantigens translocate into ABs in the process of apoptosis induced by oxidative stress. The cytoskeletal protein activation pathway and the JNK-related apoptosis pathway are involved in the transport of autoantigens and the formation of ABs. ABs may be the key bridge between MC cell apoptosis and cellular immunity.
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Casciola-Rosen, Livia, Kanneboyina Nagaraju, Paul Plotz, Kondi Wang, Stuart Levine, Edward Gabrielson, Andrea Corse, and Antony Rosen. "Enhanced autoantigen expression in regenerating muscle cells in idiopathic inflammatory myopathy." Journal of Experimental Medicine 201, no. 4 (February 21, 2005): 591–601. http://dx.doi.org/10.1084/jem.20041367.

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Unique autoantibody specificities are strongly associated with distinct clinical phenotypes, making autoantibodies useful for diagnosis and prognosis. To investigate the mechanisms underlying this striking association, we examined autoantigen expression in normal muscle and in muscle from patients with autoimmune myositis. Although myositis autoantigens are expressed at very low levels in control muscle, they are found at high levels in myositis muscle. Furthermore, increased autoantigen expression correlates with differentiation state, such that myositis autoantigen expression is increased in cells that have features of regenerating muscle cells. Consistent with this, we found that cultured myoblasts express high levels of autoantigens, which are strikingly down-regulated as cells differentiate into myotubes in vitro. These data strongly implicate regenerating muscle cells rather than mature myotubes as the source of ongoing antigen supply in autoimmune myositis. Myositis autoantigen expression is also markedly increased in several cancers known to be associated with autoimmune myositis, but not in their related normal tissues, demonstrating that tumor cells and undifferentiated myoblasts are antigenically similar. We propose that in cancer-associated myositis, an autoimmune response directed against cancer cross-reacts with regenerating muscle cells, enabling a feed-forward loop of tissue damage and antigen selection. Regulating pathways of antigen expression may provide unrecognized therapeutic opportunities in autoimmune diseases.
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Mauvais, François-Xavier, Julien Diana, and Peter van Endert. "Beta cell antigens in type 1 diabetes: triggers in pathogenesis and therapeutic targets." F1000Research 5 (April 22, 2016): 728. http://dx.doi.org/10.12688/f1000research.7411.1.

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Research focusing on type 1 diabetes (T1D) autoantigens aims to explore our understanding of these beta cell proteins in order to design assays for monitoring the pathogenic autoimmune response, as well as safe and efficient therapies preventing or stopping it. In this review, we will discuss progress made in the last 5 years with respect to mechanistic understanding, diagnostic monitoring, and therapeutic modulation of the autoantigen-specific cellular immune response in T1D. Some technical progress in monitoring tools has been made; however, the potential of recent technologies for highly multiplexed exploration of human cellular immune responses remains to be exploited in T1D research, as it may be the key to the identification of surrogate markers of disease progression that are still wanting. Detailed analysis of autoantigen recognition by T cells suggests an important role of non-conventional antigen presentation and processing in beta cell-directed autoimmunity, but the impact of this in human T1D has been little explored. Finally, therapeutic administration of autoantigens to T1D patients has produced disappointing results. The application of novel modes of autoantigen administration, careful translation of mechanistic understanding obtained in preclinical studies and in vitro with human cells, and combination therapies including CD3 antibodies may help to make autoantigen-based immunotherapy for T1D a success story in the future.
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Rosen, A., L. Casciola-Rosen, and J. Ahearn. "Novel packages of viral and self-antigens are generated during apoptosis." Journal of Experimental Medicine 181, no. 4 (April 1, 1995): 1557–61. http://dx.doi.org/10.1084/jem.181.4.1557.

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Immune context is an essential determinant of the host response to potential autoantigens. The clustering of the autoantigens targeted in systemic lupus erythematosus within surface blebs of apoptotic cells generates high concentrations of autoantigen within discrete subcellular packages. We demonstrate here that when apoptosis is induced by Sindbis virus infection, viral antigens and autoantigens cocluster exclusively in small surface blebs of apoptotic cells. The surface of these blebs is rich in viral glycoproteins, and virions can be seen blebbing from their surface. We propose that these blebs of mixed foreign and self-origin define a novel immune context that may challenge self-tolerance.
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Більше джерел

Дисертації з теми "Autoantigeni"

1

AZZONI, ELISABETTA. "IDENTIFICAZIONE DI AUTOANTIGENI IN PATOLOGIE NEUROLOGICHE AUTOIMMUNI." Doctoral thesis, Università degli studi di Trieste, 2005. http://hdl.handle.net/10077/14657.

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RUSSO, LUCIA. "Ricerca di nuovi autoantigeni nel diabete di tipo 1:immunoproteomica delle isole pancreatiche umane." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/209587.

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Introduction: Type 1 Diabetes is the autoimmune form of diabetes mellitus and accounts for about 5-10% of all cases of diabetes. It is one of the most common severe chronic childhood illnesses characterized by insulin deficiency as a result of the progressive T-cell mediated destruction of pancreatic Langerhans islet - cells. The factors initiating the destructive process are largely unknown but genetic and nongenetic factors are involved. It manifests a biphasic progression with a preclinical phase “insulitis” and a clinical phase “diabetes onset”. The preclinical phase is also characterized by the presence of circulating autoAbs targeted to a different, yet limited, series of molecules that are expressed specifically and unspecifically in the pancreatic islet -cells. To date, 5 are the known autoAbs: ICA (Islets Cell Ab), GADA (Glutammic Acid Decarboxylase 65kDa Ab), IA-2A (Tyrosin phosphatase-like insulinoma Ag 2 Ab), IAA (Insulin Ab), ZnT8A (Cation efflux Zinc Transporter 8 Ab). Search for T1D-autoAbs in patients with recent diagnosis of diabetes is utilized for diagnostic purposes, and in first-degree relatives as predictive markers of disease. The first type of autoAb, islet-cell autoantibody, “ICA” was described >35 years ago; however, the entire panel of T1D-autoAgs is not complete at the moment. For example, it has been recently (2007) identified a new major autoAg, ZnT8, that was found in 26% of T1D subjects previously classified as autoAbs-negative. Because up to 5% of children with the clinical features/diagnosis of T1D test negative for known autoAbs it is likely that other specific autoAbs/Ags remain to be identified. Aim: We set up a search for new autoantigens involved in T1D using a method that has to be considered innovative in its application to this organ-specific autoimmune disease, that we named immunoproteomic approach; in addition we developed a radioimmunobinding assay to the goal of detecting serum reactivity on a large-scale as validation of two new potential autoantigen molecules identified by immunoproteomic. Materials and Methods: We studied the autoantibody repertoire of subject with diabetes of early onset (1- 10 years of age), divided in different groups of sera: A1) Subjects with diabetes negative to all autoAbs (ICA, GADA, IA-2A, IAA, ZnT8A) and to the search for mutations in neonatal diabetes genes -INS, KCNJ11, ABCC8 and GCK- (5 sera); B) T1D subjects positive only to IAA (4 sera); C) T1D subjects positive only to ZnT8A (4sera) and D) T1D subjects positive only to GADA and IA-2A (8 sera). Sera from patients with diabetes due to insulin mutations were used as “negative” control (group E1). The reactivity of these sera was tested against cytoplasmic/membrane-enriched protein fraction from human pancreatic islets or from exocrine pancreas sera in order to exclude any source of contamination of pancreatic islets from this tissue. After bidimensional electrophoresis and classical Western Blot, images were acquired and spot detection/matching performed by Progenesis software. Spots revealed by control sera (group E1) were subtracted as “noise” in each categories of T1D-sera. For matching the reactivity between groups of sera we detected specific spots of each group and common spots to two or more groups of the type 1 diabetic patients. These spots were identified on the corresponding stain gel by Mass Spectrometry. Among identified protein spots of islets two molecules (IOH-X1 and IOH-X2) were chosen to be validated as new potential autoAgs with a “radioimmunobinding assay” in subjects with T1D developed early (≤10 years of age). We studied IOH-X1 in five constructs (ORF: aa 1-445; N-terminal: aa 1-125; Domain 2: aa 120-225; Central Fragment: aa 215-337 and C-terminal: aa 338-445), whereas IOH-X2 in three constructs (ORF: aa 1-165; N-terminal: aa1-80 and C-terminal: aa 75-165). ORF and selected constructs were amplified by PCR from corresponding human islet cDNA using specific coupled of primers. They were cloned in an eucariotic vector and then expressed in an in vitrocoupled transcription/translation reticulocyte lysate reaction in presence of a radioactive aminoacid (MetS35). The products purified on a sephadex column were used with human serum samples of diabetic and control patients in an immunoprecipitation assay and finally the radioactivity was valued by an appropriate instrument. Results: Matching revealed that among protein spots detected in pancreatic islet cytoplasmic/membraneenriched protein fraction, 10 were in common between negative to 5 autoAbs sera (group A1) and those IAA positive (group B), 24 were in common between group A1 and those ZnT8A positive sera (group C) and 14 spots were common to all three groups. We then proceeded to identifying these protein spots by MALDI MS/MS. Our initial analysis revealed the IOH-X1 protein among spots detected by all groups of T1D-sera and the IOH-X2 molecule among protein spots detected only by the negative to 5 autoAb sera group. Among potential autoantigens we also identified tubulins, a common spot by all three groups of sera, and the Protein disulfide isomerase/PDIA3, as a specific spot of ZnT8A positive sera group. Tubulins and PDI are known as uncommon antigens in T1D, already identified by others. To confirm protein identity of spots we performed a preliminary validation by Western Blot. We recognized with protein-specific primary antibodies the corresponding spots that were picked and identified on stain-gel by Maldi MS/MS as IOH-X1 and IOH-X2. At the same time, to confirm the robustness of our method, we set up the detection of a known autoAg spot by using GADA positive sera and subsequently a polyclonal anti-GAD65 antibody on the same nitrocellulose. In our preliminary study we tested only the ORF and the C-terminal construct of IOH-X1 protein whereas the others remain to be analysed. In the C-terminus assay, applied on 100 patients with type 1 diabetes, 100 controls (obese) and 100 children with coeliac disease, when the 99° percentile cut-off was utilized, we found that 24% patients with T1D and 9% patients with coeliac disease were positive to the assay. Conclusions: These results seem to indicate that our “immunoproteomic” method can detect known T1D autoantigens as well as it’s feasible for novel autoantigens identification. Further analysis remain to be performed to assess if these potential new biomarkers may be useful to improving the accuracy of T1D diagnosis in high risk patients and general population, and to provide new targets for tolerance induction strategies
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Blöcker, Inga-Madeleine. "Epitopmapping des epidermalen Autoantigens BP230." Lübeck Zentrale Hochschulbibliothek Lübeck, 2010. http://d-nb.info/1003311334/34.

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4

Schumann, Frank. "Autoantigene bei der rheumatoiden Arthritis." [S.l.] : [s.n.], 2004. http://www.diss.fu-berlin.de/2004/199/index.html.

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Raith, Albert Johann. "Charakterisierung des potenziellen Autoantigens cRALBP." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-47172.

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6

Frazer, Hilary Elizabeth. "Autoantigens in connective tissue disease." Thesis, Queen's University Belfast, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328058.

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7

Tengnér, Pia. "Immune responses to the Ro and La autoantigens /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3590-4/.

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8

Mewar, Devesh. "Studies on autoantigens in rheumatoid arthritis." Thesis, University of Sheffield, 2003. http://etheses.whiterose.ac.uk/3455/.

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This thesis describes the use of phage display for the isolation of autoantigens in rheumatoid arthritis. The potential of the technology is demonstrated by the isolation of an autoantigen, eukaryotic translation elongation factor 1a1 (eEF 1 (x 1)) from a fibroblast cDNA library using rounds of selective enrichment with IgG from RA patients. Subsequently in order to isolate joint-specific antigens a phage-displayed cDNA library from rheumatoid pannus was generated and screened with analogous procedures. From the clones isolated, putative candidate autoantigens were identified. The presence of anti- eEF 1a1 autoantibodies in approximately 20% of patients with RA was confirmed and extended in larger panels of sera, and the finding of anti-eEF la1 shown to be relatively specific for RA. In contrast autoantibodies to the activation-induced negative regulator of T cells, CTLA-4 were not found in contrast to a previous report. The relevance of these findings for the use of antibodies in the diagnosis and prediction of disease characteristics in RA are discussed.
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9

Iwobi, Mabel Uzoamaka. "Salivary autoantigens in human rheumatic diseases." Thesis, University of Sussex, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260048.

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10

Ciudad, García María Teresa. "Autoantigen Processing. How immunodominant thyroglobulin peptides are generated and presented by HLA-DR molecules." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/325144.

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Las células dendríticas (DC) son las APCs más capaces, expresan toda la maquinaria necesaria y tienen una gran capacidad de presentación eficaz. Hemos establecido que el peptidoma de APCs profesionales puede ser estudiado sin tener que recurrir a líneas celulares, usando un pequeño número de DCs derivadas de monocitos que tienden a seleccionar péptidos de muy alta afinidad que forman familias de péptidos (nested sets) como norma. Sin embargo, también presentan péptidos no convencionales. 20% de los péptidos presentados por todos los alelos eran péptidos N o C terminales. La mayoría de los C terminales se encuentran justo en el extremo de la proteína, proceden de proteínas citosólicas y no se agrupan en nested sets. También muestran residuos preferentes de corte enzimático, en comparación con los péptidos internos. Hemos utilizado moDCs y un modelo in vitro de digestión en un sistema "libre de células" (CFS) para analizar el procesamiento y la presentación de un autoantígeno tiroideo, la tiroglobulina. Tiroglobulina nativa o desnaturalizada capturada por MoDC generó muchos péptidos, con nested sets dominantes y ningún péptido derivado de los N o C terminales de la proteína. Se obtuvo un patrón similar cuando las DC se pulsaron con extractos de tejido tiroideo. Sin embargo, si la tiroglobulina se digería por las catepsinas coloidales (B, L y S) a pH 7,4 antes de pulsar las DCs, la presentación de péptidos de tiroglobulina quedó casi completamente eliminada. La gran cantidad de tiroglobulina intacta en el extracto de tejido podría ser la causa de estos datos y que la pre-digestión debe haber destruido todos los epítopos de tiroglobulina capaces de ser presentados. Sin embargo, cuando hicimos el mismo experimento utilizando el CFS, la tiroglobulina predigerida se presentó tan eficientemente como la proteína purificada. Por lo tanto, la pre-digestión no destruye los epítopos, pero en las DC los fragmentos pueden haber sido degradados antes de llegar al MIIC. Por lo tanto, el estado del antígeno es extremadamente relevante para su presentación por DCs pero el método CFS puede ayudar a identificar etapas del procesamiento que se pueden perder en el análisis de péptidos presentados por DC. Dos nested sets abundantes, de alta afinidad afinidad y dominantes de la tiroglobulina fueron identificados. Uno, asociado a HLA-DR3 con el core VVVDPSIRH y uno asociado a HLA-DR15 con el core IMQYFSHFI. El grupo VVVDPSIRH contiene el péptido Tg2098, definido como inmunodominante en un modelo in vivo de tiroiditis en ratones transgénicos HLA-DR3. El mismo péptido se identificó en el peptidoma de tiroides de pacientes de Graves' HLA-DR3+. HLA-DR15 no se asocia negativamente a tiroiditis pero en un modelo similar, ratones transgénicos HLA-DR15 no desarrollaron la enfermedad usando las mismas condiciones. Curiosamente, en DCs HLA-DR15/DR3, la mayoría de los péptidos de tiroglobulina fueron presentados por HLA-DR15 pero péptidos con este core no se encontraron en muestras de tiroides HLA-DR15+ afectados. También se encontró un segundo nested set asociado a HLA-DR3, independiente de la fuente de antígeno o el método de procesamiento. Este segundo nested set, alrededor del core VIFDANAPV, no era tan abundante como el VVVDPSIRH y contenía un péptido (Tg1574), conocido por no generar respuestas de células T en el mismo modelo que el péptido Tg2098. La diferencia funcional entre estos dos péptidos correlacionaron con dos características que son importantes en la definición de inmunodominancia, es decir, la sensibilidad a las catepsinas y a HLA-DM. Tg1574 era resistente a catepsinas mientras que Tg2098 era parcialmente sensible. Tras la digestión con varias combinaciones de catepsinas, Tg1574 no generó variantes intermedias. Sin embargo, Tg2098 fue recortado en los extremos, generando una serie de variantes, su core se mantuvo resistente a la proteolisis. Además, Tg1574 era mucho más sensible a HLA-DM que Tg2098. La interpretación de estos datos y la identificación de cuál de los dos péptidos de tiroglobulina se presenta preferentemente en el timo, serán necesarios para demostrar plenamente nuestra hipótesis.
DCs are the most capable APCs, express all the necessary machinery and have a high capacity of efficient presentation. We have established that the peptidome from unpulsed professional APC can be studied without having to resort to cell lines, using small numbers of monocyte-derived DCs that tend to select very high-affinity peptides forming nested sets as a norm. However, they also presented unconventional peptides. 20% of the peptides presented by all alleles were N-terminal or C-terminal peptides. Most C-terminal peptides were located at the very extreme of the protein, pertained to cytosolic proteins and did not cluster in nested sets. They also show preferent cleavage residues, compared to internal peptides. We have used MoDCs and an in vitro digestion model set up as a cell-free system (CFS) to analyze the processing and presentation of an AITD autoantigen, thyroglobulin. Native or denatured purified thyroglobulin captured by MoDC generated many peptides, with dominant nested sets and no peptide derived from the N- or C-terminus of the protein. Very similar pattern was obtained wen MoDC were pulsed with colloid-enriched thyroid tissue extracts. Yet, if thyroglobulin was digested by the colloid cathepsins (B, L and S) at pH 7.4 prior to pulsing, MoDCs presentation of thyroglobulin peptides was almost completely abrogated. The large amount of intact thyroglobulin in the tissue extract could be accountable for these data and that the pre-digestion must have destroyed any thyroglobulin epitope that could be presented. However, when we did the same experiment using the CFS, predigested thyroglobulin was as efficiently presented as purified protein. Therefore, pre-digestion did not destroy epitopes, the fragments may have been degraded before reaching the MIIC in MoDCs. Thus, the state of the antigen is extremely relevant for its presentation by MoDCs but, the CFS method may help identifying steps of the processing events that may be lost when analyzing DC-presented peptides. Two abundant and high affinity dominant nested sets were identified from thyroglobulin. One, associated to HLA-DR3 with the VVVDPSIRH core and one associated to HLA-DR15 with the core IMQYFSHFI. The VVVDPSIRH set contains peptide Tg2098, defined as immunodominant in an in vivo model of thyroiditis in HLA-DR3 transgenic mice. The same peptide was identified in the HLA-DR3+ peptidome from GD patients' thyroids. HLA-DR15 is not negatively associated to AITD but in a similar model, HLA-DR15 transgenic mice did not develop the disease using the same conditions. Interestingly, in HLA-DR15/DR3 MoDCs, most thyroglobulin peptides were presented by HLA-DR15 but peptides with this core were not identified in HLA-DR15+ thyroid samples affected by GD. A second nested set associated to HLA-DR3 was also found, independent of the source of antigen or the processing method. This second HLA-DR3 nested set, around the VIFDANAPV core, was not as abundant as the VVVDPSIRH and contained a peptide (Tg1574), known not to generate T cell responses in the same EAT model as the Tg2098 peptide. The functional difference between these two peptides correlated with two characteristics that are important in the definition of immunodominance, i.e. sensitivity to cathepsins and to HLA-DM. Tg1574 was cathepsin-resistant whereas Tg2098 was partially sensitive. Upon digestion with several combinations of cathepsins, Tg1574 did not generate any intermediate variants and between 45 and 100% remained intact. In contrast, Tg2098 was trimmed at the peptide ends generating a number of variants, its core was maintained resistant to cleavage and only between 6 and 26% remained intact. In addition, Tg1574 was much more sensitive to HLA-DM than Tg2098. Interpreting these data after identifying what of the two peptides is preferentially presented in thymus will be necessary to fully demonstrate our hypothesis.
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Книги з теми "Autoantigeni"

1

Martin, Alberto. Epitope studies on the human autoantigen, histidyl-tRNA synthetase. Ottawa: National Library of Canada, 1994.

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2

Brand, Stephen Robert. Autoantigenic and structural analysis of the proliferating cell nuclear antigen. Manchester: University of Manchester, 1993.

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3

Davies, Marie Louise. Autoantigen specific T cell responses in relation to systemic lupus erythematosus. Birmingham: University of Birmingham, 2000.

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4

Superoxid-Dismutase vom Mangan-Typ als Autoantigen bei akuter Epstein-Barr-Virus-Infektion. Göttingen: Cuvillier, 1996.

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5

Dumont, Caroline R. Identifying the autoantigen of a diabetogenic CD8 T cell clone isolated from Young NOD mice. [New Haven, Conn: s.n.], 1999.

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6

1953-, Eden Willem van, ed. Heat shock proteins and inflammation. Basel: Birkhäuser Verlag, 2003.

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7

Dresden Symposium on Autoantibodies (5th 2000 Dresden, Germany). Autoantigens and autoantibodies: Diagnostic tools and clues to understanding autoimmunity : report on the 5th Dresden Symposium on Autoantibodies held in Dresden on October 18-21, 2000. Lengerich: Pabst Science Publishers, 2000.

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8

S, Eisenbarth George, ed. Endocrine and organ specific autoimmunity. Austin, Tex., U.S.A: RlG. Landes Co., 1999.

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9

Winqvist, Ola. Autoantigens in Addison's Disease. Almqvist & Wiksell Internat., 1994.

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10

Frazer, Hilary Elizabeth. Autoantigens in connective tissue disease. 1986.

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Частини книг з теми "Autoantigeni"

1

Stöcker, W. "Autoantigene." In Springer Reference Medizin, 237. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_344.

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2

Stöcker, W. "Autoantigene." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_344-1.

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3

Holsapple, Michael. "Autoantigens." In Encyclopedia of Immunotoxicology, 89–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_136.

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4

Steiner, Günter, and Karsten Conrad. "Autoantigene." In Molekularmedizinische Grundlagen von rheumatischen Erkrankungen, 123–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55803-0_6.

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5

Weetman, Anthony P., E. Helen Kemp, Jonathan N. Ridgway, and Philip F. Watson. "Orbital Autoantigens." In Thyroid Eye Disease, 1–20. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1447-3_1.

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6

Leung, Patrick S. C., Ian Mackay, and M. Eric Gershwin. "Mitochondrial autoantigens." In Manual of Biological Markers of Disease, 543–56. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-1670-1_35.

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7

Ludgate, M. "Thyroid autoantigens." In Endocrine Autoimmunity and Associated Conditions, 25–38. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5044-6_2.

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8

Leung, Patrick S. C., Ian Mackay, and M. Eric Gershwin. "Mitochondrial autoantigens." In Manual of Biological Markers of Disease, 530–59. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-5444-4_19.

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9

Tomiyama, Yoshiaki. "Autoantigens in ITP." In Autoimmune Thrombocytopenia, 53–62. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4142-6_5.

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10

Nishimori, Isao, and Michael A. Hollingsworth. "Autoantigens of Sjögren’s Syndrome." In Autoimmune Reactions, 61–77. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-4612-1610-0_5.

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Тези доповідей конференцій з теми "Autoantigeni"

1

Mohammad, A., A. Starastsin, and D. Nizheharodava. "THE COMPARISON OF INTRAEPITHELIAL LYMPHOCYTES IN SMALL AND LARGE INTESTINE OF CROHN’S DISEASE PATIENTS." In SAKHAROV READINGS 2021: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2021. http://dx.doi.org/10.46646/sakh-2021-2-79-82.

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The changes in intraepithelial lymphocytes phenotype of the small and large intestine were established in patients with Crohn’s disease what may be used as a hallmark of immune inflammation in the gut and make intraepithelial lymphocytes ideal candidate for targeting in further immunoregulation of mucosal adaptive immune response against autoantigens.
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2

Sanchez, Tino Wilson, Guangyu Zhang, Jitian Li, Liping Dai, Saied Mirshahidi, Nathan R. Wall, Clayton Yates, et al. "Abstract 1130: Targeting the tumor-associated autoantigen alpha-enolase in prostate cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1130.

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3

Corsiero, E., L. Jagemann, E. Prediletto, C. Pitzalis, and M. Bombardieri. "OP0175 Characterization of novel stromal-derived autoantigens recognized by ra synovial monoclonal antibodies." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3870.

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4

Suzuki, M., M. Hirakata, A. Suwa, T. Nojima, H. Yasuoka, S. Satoh, T. Fujii, S. Inada, and T. Mimori. "THU0067 Analysis of autoantigens recognised by autoantibodies that immunoprecipitate high molecular weight nucleic acids." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.911.

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5

Suwa, A., M. Hirakata, T. Nojima, S. Satoh, T. Nakajima, and T. Mimori. "THU0066 Autoantigenic epitopes targeted by autoantibodies to rna helicase a in systemic lupus erythematosus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.910.

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6

de Moel, E. C., L. Rozeman, A. Grummels, E. M. E. Verdegaal, J. A. Bakker, E. H. Kapiteijn, T. W. J. Huizinga, J. B. Haanen, R. E. M. Toes, and D. van der Woude. "THU0024 Treatment with immune checkpoint inhibitors and the break of b-cell tolerance to autoantigens." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3017.

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7

Tsekhanovich, D., A. Starastsin, A. Dybau, and D. Nizheharodava. "Y6T-LYMPHOCYTES PHENOTYPE IN PATIENTS WITH INFLAMMATORY BOWEL DISEASES." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-68-71.

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YST-сells role in inflammatory bowel disease is still not fully investigated: on the one hand, they are thought to be involved in dysregulation of the immune response to gastrointestinal commensal bacteria in genetically susceptible individuals and, on the other hand, YST-cells may initiate repair of damaged intestinal epithelium and exhibit immunoreg-ulatory effects. The composition of T-lymphocytes subsets (авТ-cells, YST-cells) and the expression of functional molecules (TLR4+, CD314+, CD8+, CD45RO+) on circulating YST-cells in patients with inflammatory bowel disease were characterized in this study. An increase of YST-cells numbers predominantly expressing a cytotoxic phenotype along with a depletion of YST-cells memory population in peripheral blood of patients with Crohn’s disease and ulcerative colitis has been shown, what may reflect impaired tolerance mechanisms and results from chronic stimulation to autoantigens.
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8

Marklein, B., M. Jenning, K. Muenzer, G. Burmester, and K. Skriner. "SAT0004 New autoantigen (JKTBP) part of stress granules closes the sensitivity gap in rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3653.

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9

Marklein, Bianka, Madeleine Jenning, Karen Münzner, Zoltan Konthur, Thomas Häupl, Andrew Cope, Mark Shlomchik, et al. "02.41 New autoantigen (jktbp) part of stress granules closes the sensitivity gap in rheumatoid arthritis." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211050.41.

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10

Schulz-Knappe, PK, P. Budde, H.-D. Zucht, D. Wirtz, K. Marquardt, R. Thomas, T. Witte, M. Schneider, K. Sivils, and A. Rasmussen. "OP0333 Discovery and validation of novel autoantigens in sjÖgren's syndrome with potential for subgrouping of disease." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5725.

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Звіти організацій з теми "Autoantigeni"

1

Racevskis, Janis. Detection and Characterization of Autoantigens in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada299494.

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