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[PMID]:29412476
[Au] Autor:Bakela K; Dimakopoulou M; Batsou P; Manidakis N; Athanassakis I
[Ad] Endereço:Laboratory of Immunology, Department of Biology, University of Crete, Heraklion, Crete, Greece.
[Ti] Título:Soluble MHC class II-driven therapy for a systemic lupus erythematosus murine experimental in vitro and in vivo model.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Taking into consideration the multiparametric nature of systemic lupus erythematosus (SLE), the severity and variability of symptoms and the lack of effective therapeutic approaches, this study took advantage of the recently described role of soluble major histocompatibility complex class II (sMHCII) molecules in maintaining tolerance to the organism and attempted to apply sMHCII proteins as a treatment to murine SLE experimental models in vitro as well as in vivo. After breaking tolerance to DNA in vitro, which was accompanied by development of specific anti-dsDNA antibodies, syngeneic or allogeneic sMHCII molecules, purified from healthy mouse serum, could significantly reduce the specific antibody levels and drive the system towards immunosuppression, as assessed by specific marker analysis on T cells and cytokine production by flow cytometry and ELISA, respectively. The in vivo experimental model consisted of pristane-induced SLE symptoms to BALB/c mice, which developed maximal levels of anti-dsDNA 2 months after pristane inoculation. Syngeneic or allogeneic sMHCII administration could alleviate pristane-induced symptoms, significantly decrease specific anti-dsDNA antibody production and develop immunosuppression to the host, as manifested by increase of CD4 + CTLA-4 +  and CD4 + CD25 +  cell populations in the spleen. Thus, the results presented in this study introduced the ability of sMHCII proteins to suppress specific autoantigen response, opening new areas of research and offering novel therapeutic approaches to SLE with expanding features to other autoimmune diseases.
[Mh] Termos MeSH primário: Anticorpos Antinucleares/imunologia
Autoantígenos/imunologia
Antígenos de Histocompatibilidade Classe II/imunologia
Tolerância Imunológica/imunologia
Imunoterapia/métodos
Lúpus Eritematoso Sistêmico/imunologia
Lúpus Eritematoso Sistêmico/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD4/metabolismo
Antígeno CTLA-4/metabolismo
Células Cultivadas
DNA/imunologia
Modelos Animais de Doenças
Imunossupressão
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Lúpus Eritematoso Sistêmico/induzido quimicamente
Camundongos
Camundongos Endogâmicos BALB C
Baço/citologia
Baço/imunologia
Terpenos/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Autoantigens); 0 (CD4 Antigens); 0 (CTLA-4 Antigen); 0 (Histocompatibility Antigens Class II); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Terpenes); 26HZV48DT1 (pristane); 9007-49-2 (DNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12644


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[PMID]:27775687
[Au] Autor:Iwata H; Kamaguchi M; Ujiie H; Nishimura M; Izumi K; Natsuga K; Shinkuma S; Nishie W; Shimizu H
[Ad] Endereço:Department of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
[Ti] Título:Macropinocytosis of type XVII collagen induced by bullous pemphigoid IgG is regulated via protein kinase C.
[So] Source:Lab Invest;96(12):1301-1310, 2016 12.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macropinocytosis is an endocytic pathway that is involved in the nonselective fluid uptake of extracellular fluid. Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease associated with autoantibodies to type XVII collagen (COL17), which is a component of hemidesmosome. When keratinocytes are treated with BP-IgG, COL17 internalizes into cells by way of the macropinocytosis. We investigated the mechanism of COL17 macropinocytosis using DJM-1 cells, a cutaneous squamous cell carcinoma cell line. First, non-hemidesmosomal COL17 was preferentially depleted by stimulation with the BP-IgG in the DJM-1 cells. To investigate the signaling involved in COL17-macropinocytosis, the inhibition of small GTPase family members Rac1 and Cdc42 was found to strongly repress COL17 internalization; in addition, the Rho inhibitor also partially blocked that internalization, suggesting these small GTPases are involved in signaling to mediate COL17-macropinocytosis. Western blotting using Phostag-SDS-PAGE demonstrated high levels of COL17 phosphorylation in DJM-1 cells under steady-state condition. Treatment with BP-IgG increased the intracellular calcium level within a minute, and induced the overabundant phosphorylation of COL17. The overabundant phosphorylation of COL17 was suppressed by a protein kinase C (PKC) inhibitor. In addition, PKC inhibitor repressed COL17 endocytosis using cell culture and organ culture systems. Finally, the depletion of COL17 was not observed in the HEK293 cells transfected COL17 without intracellular domain. These results suggest that COL17 internalization induced by BP-IgG may be mediated by a PKC pathway. In summary, BP-IgG initially binds to COL17 distributed on the plasma membrane, and COL17 may be internalized by means of a macropinocytic pathway related to the phosphorylation of the intracellular domain by PKC.
[Mh] Termos MeSH primário: Autoanticorpos/farmacologia
Autoantígenos/metabolismo
Imunoglobulina G/farmacologia
Queratinócitos/efeitos dos fármacos
Colágenos não Fibrilares/metabolismo
Penfigoide Bolhoso/imunologia
Pinocitose/efeitos dos fármacos
Proteína Quinase C/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Autoantígenos/química
Autoantígenos/genética
Sinalização do Cálcio/efeitos dos fármacos
Linhagem Celular Tumoral
Células HEK293
Seres Humanos
Queratinócitos/imunologia
Queratinócitos/metabolismo
Queratinócitos/patologia
Camundongos
Colágenos não Fibrilares/química
Colágenos não Fibrilares/genética
Penfigoide Bolhoso/metabolismo
Penfigoide Bolhoso/patologia
Fragmentos de Peptídeos
Fosforilação/efeitos dos fármacos
Domínios e Motivos de Interação entre Proteínas
Proteína Quinase C/antagonistas & inibidores
Inibidores de Proteínas Quinases/farmacologia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Proteínas Recombinantes
Técnicas de Cultura de Tecidos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Autoantibodies); 0 (Autoantigens); 0 (Immunoglobulin G); 0 (Non-Fibrillar Collagens); 0 (Peptide Fragments); 0 (Protein Kinase Inhibitors); 0 (Recombinant Proteins); 0 (collagen type XVII); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2016.108


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[PMID]:28470667
[Au] Autor:Tanaka T; Zhang W; Sun Y; Shuai Z; Chida AS; Kenny TP; Yang GX; Sanz I; Ansari A; Bowlus CL; Ippolito GC; Coppel RL; Okazaki K; He XS; Leung PSC; Gershwin ME
[Ad] Endereço:Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, Davis, CA.
[Ti] Título:Autoreactive monoclonal antibodies from patients with primary biliary cholangitis recognize environmental xenobiotics.
[So] Source:Hepatology;66(3):885-895, 2017 09.
[Is] ISSN:1527-3350
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major problem in autoimmunity has been identification of the earliest events that lead to breach of tolerance. Although there have been major advances in dissecting effector pathways and the multilineage immune responses to mitochondrial self-antigens in primary biliary cholangitis, the critical links between environmental factors and tolerance remain elusive. We hypothesized that environmental xenobiotic modification of the E2 subunit of the pyruvate dehydrogenase (PDC-E2) inner lipoyl domain can lead to loss of tolerance to genetically susceptible hosts. Previously we demonstrated that serum anti-PDC-E2 autoantibodies cross-react with the chemical xenobiotics 2-octynoic acid and 6,8-bis (acetylthio) octanoic acid and further that there is a high frequency of PDC-E2-specific peripheral plasmablasts. Herein we generated 104 recombinant monoclonal antibodies (mAbs) based on paired heavy-chain and light-chain variable regions of individual plasmablasts derived from primary biliary cholangitis patients. We identified 32 mAbs reactive with native PDC-E2, including 20 specific for PDC-E2 and 12 cross-reactive with both PDC-E2 and 2-octynoic acid and 6,8-bis (acetylthio) octanoic acid. A lower frequency of replacement somatic hypermutations, indicating a lower level of affinity maturation, was observed in the complementarity-determining regions of the cross-reactive mAbs in comparison to mAbs exclusively recognizing PDC-E2 or those for irrelevant antigens. In particular, when the highly mutated heavy-chain gene of a cross-reactive mAb was reverted to the germline sequence, the PDC-E2 reactivity was reduced dramatically, whereas the xenobiotic reactivity was retained. Importantly, cross-reactive mAbs also recognized lipoic acid, a mitochondrial fatty acid that is covalently bound to PDC-E2. CONCLUSION: Our data reflect that chemically modified lipoic acid or lipoic acid itself, through molecular mimicry, is the initial target that leads to the development of primary biliary cholangitis. (Hepatology 2017;66:885-895).
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Autoantígenos/imunologia
Autoimunidade/genética
Colangite/imunologia
Colangite/patologia
Xenobióticos/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais/metabolismo
Autoantígenos/genética
Autoimunidade/imunologia
Feminino
Amplificação de Genes
Seres Humanos
Immunoblotting
Masculino
Mimetismo Molecular/genética
Reação em Cadeia da Polimerase em Tempo Real
Sensibilidade e Especificidade
Ácido Tióctico/imunologia
Ácido Tióctico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Autoantigens); 0 (Xenobiotics); 73Y7P0K73Y (Thioctic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/hep.29245


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[PMID]:29274781
[Au] Autor:Liu D; Qian W; Li D; Kong L
[Ad] Endereço:Department of Gastroenteology and Hepatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. Electronic address: danliu666@hotmail.com.
[Ti] Título:Ro60/SSA levels are increased and promote the progression of pancreatic ductal adenocarcinoma.
[So] Source:Biochem Biophys Res Commun;495(4):2519-2524, 2018 01 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ro60/SSA is a vital auto antigen that is targeted in Sjogren's syndrome and systemic lupus erythematosus (SLE). However, its role in solid cancers has rarely been reported. The present study investigated the expression and function of Ro60/SSA in the development of pancreatic ductal adenocarcinoma (PDAC) both in vitro and in vivo. Immunohistochemistry was used to examine the expression of Ro60/SSA in PDAC and normal pancreatic tissues by using tissue microarray chips. The results showed that Ro60/SSA expression was increased in PDAC tissues compared with normal pancreatic tissues. Knockdown of Ro60/SSA by siRNA transfection significantly decreased cell proliferation and invasion in vitro. Furthermore, knockdown of Ro60/SSA inhibited the growth of subcutaneous tumors in vivo. Taken together, the current study provides evidence of new function of Ro60/SSA in the development of cancer. It facilitates pancreatic cancer proliferation, migration and invasion. Therefore, it may represent a novel molecular target for the management of pancreatic cancer.
[Mh] Termos MeSH primário: Autoantígenos/metabolismo
Carcinoma Ductal Pancreático/metabolismo
Carcinoma Ductal Pancreático/patologia
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
RNA Citoplasmático Pequeno/metabolismo
Ribonucleoproteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Células Tumorais Cultivadas
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (RNA, Small Cytoplasmic); 0 (Ribonucleoproteins); 0 (TROVE2 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


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[PMID]:29320567
[Au] Autor:Gil-Cayuela C; Ortega A; Tarazón E; Martínez-Dolz L; Cinca J; González-Juanatey JR; Lago F; Roselló-Lletí E; Rivera M; Portolés M
[Ad] Endereço:Cardiocirculatory Unit, Health Research Institute of La Fe University Hospital (IIS La Fe), Valencia, Spain.
[Ti] Título:Myocardium of patients with dilated cardiomyopathy presents altered expression of genes involved in thyroid hormone biosynthesis.
[So] Source:PLoS One;13(1):e0190987, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The association between dilated cardiomyopathy (DCM) and low thyroid hormone (TH) levels has been previously described. In these patients abnormal thyroid function is significantly related to impaired left ventricular (LV) function and increased risk of death. Although TH was originally thought to be produced exclusively by the thyroid gland, we recently reported TH biosynthesis in the human ischemic heart. OBJECTIVES: Based on these findings, we evaluated whether the genes required for TH production are also altered in patients with DCM. METHODS: Twenty-three LV tissue samples were obtained from patients with DCM (n = 13) undergoing heart transplantation and control donors (n = 10), and used for RNA sequencing analysis. The number of LV DCM samples was increased to 23 to determine total T4 and T3 tissue levels by ELISA. RESULTS: We found that all components of TH biosynthesis are expressed in human dilated heart tissue. Expression of genes encoding thyroperoxidase (-2.57-fold, P < 0.05) and dual oxidase 2 (2.64-fold, P < 0.01), the main enzymatic system of TH production, was significantly altered in patients with DCM and significantly associated with LV remodeling parameters. Thyroxine (T4) cardiac tissue levels were significantly increased (P < 0.01), whilst triiodothyronine (T3) levels were significantly diminished (P < 0.05) in the patients. CONCLUSIONS: Expression of TH biosynthesis machinery in the heart and total tissue levels of T4 and T3, are altered in patients with DCM. Given the relevance of TH in cardiac pathology, our results provide a basis for new gene-based therapeutic strategies for treating DCM.
[Mh] Termos MeSH primário: Autoantígenos/genética
Cardiomiopatia Dilatada/genética
Oxidases Duais/genética
Iodeto Peroxidase/genética
Proteínas de Ligação ao Ferro/genética
Miocárdio/metabolismo
Receptores da Tireotropina/genética
Hormônios Tireóideos/biossíntese
[Mh] Termos MeSH secundário: Autoantígenos/metabolismo
Biomarcadores/metabolismo
Cardiomiopatia Dilatada/patologia
Estudos de Casos e Controles
Oxidases Duais/metabolismo
Feminino
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Seres Humanos
Iodeto Peroxidase/metabolismo
Proteínas de Ligação ao Ferro/metabolismo
Masculino
Meia-Idade
Receptores da Tireotropina/metabolismo
Remodelação Ventricular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Biomarkers); 0 (Iron-Binding Proteins); 0 (Receptors, Thyrotropin); 0 (Thyroid Hormones); EC 1.11.1.- (Dual Oxidases); EC 1.11.1.7 (TPO protein, human); EC 1.11.1.8 (Iodide Peroxidase); EC 1.6.3.1 (DUOX2 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190987


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[PMID]:29175329
[Au] Autor:Yang X; Qu K; Tao J; Yin G; Han S; Liu Q; Sun H
[Ad] Endereço:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China.
[Ti] Título:Inhibition of CIP2A attenuates tumor progression by inducing cell cycle arrest and promoting cellular senescence in hepatocellular carcinoma.
[So] Source:Biochem Biophys Res Commun;495(2):1807-1814, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CIP2A is a recent identified oncogene that inhibits protein phosphatase 2A (PP2A) and stabilizes c-Myc in cancer cells. To investigate the potential oncogenic role and prognostic value of CIP2A, we comprehensively analyzed the CIP2A expression levels in pan-cancer and observed high expression level of CIP2A in majority cancer types, including hepatocellular carcinoma (HCC). Based on a validation cohort including 60 HCC and 20 non-tumorous tissue samples, we further confirmed the high mRNA and protein expression levels of CIP2A in HCC, and found high CIP2A mRNA expression level was associated with unfavorable overall and recurrence-free survival in patients with HCC. Mechanistic investigations revealed that inhibition of CIP2A significantly attenuated cellular proliferation in vitro and tumourigenicity in vivo. Bioinformatic analysis suggested that CIP2A might be involved in regulating cell cycle. Our experimental data further confirmed CIP2A knockdown induced cell cycle arrest at G1 phase. We found accumulated cellular senescence in HCC cells with CIP2A knockdown, companying expression changes of senescence associated proteins (p21, CDK2, CDK4, cyclin D1, MCM7 and FoxM1). Mechanistically, CIP2A knockdown repressed FoxM1 expression and induced FoxM1 dephosphorylation. Moreover, inhibition of PP2A by phosphatase inhibitor rescued the repression of FoxM1. Taken together, our results showed that CIP2A was highly expressed in HCC. Inhibition of CIP2A induced cell cycle arrest and promoted cellular senescence via repressing FoxM1 transcriptional activity, suggesting a potential anti-cancer target for patients with HCC.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia
Pontos de Checagem do Ciclo Celular/fisiologia
Neoplasias Hepáticas/terapia
Proteínas de Membrana/antagonistas & inibidores
[Mh] Termos MeSH secundário: Autoantígenos/genética
Autoantígenos/fisiologia
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/patologia
Pontos de Checagem do Ciclo Celular/genética
Linhagem Celular Tumoral
Senescência Celular/genética
Senescência Celular/fisiologia
Progressão da Doença
Proteína Forkhead Box M1/metabolismo
Expressão Gênica
Técnicas de Silenciamento de Genes
Células Hep G2
Seres Humanos
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/patologia
Proteínas de Membrana/genética
Proteínas de Membrana/fisiologia
Oncogenes
Prognóstico
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Neoplásico/genética
RNA Neoplásico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Biomarkers, Tumor); 0 (FOXM1 protein, human); 0 (Forkhead Box Protein M1); 0 (KIAA1524 protein, human); 0 (Membrane Proteins); 0 (RNA, Messenger); 0 (RNA, Neoplasm)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:27776542
[Au] Autor:Danan-Gotthold M; Guyon C; Giraud M; Levanon EY; Abramson J
[Ad] Endereço:The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, 52900, Israel.
[Ti] Título:Extensive RNA editing and splicing increase immune self-representation diversity in medullary thymic epithelial cells.
[So] Source:Genome Biol;17(1):219, 2016 10 24.
[Is] ISSN:1474-760X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In order to become functionally competent but harmless mediators of the immune system, T cells undergo a strict educational program in the thymus, where they learn to discriminate between self and non-self. This educational program is, to a large extent, mediated by medullary thymic epithelial cells that have a unique capacity to express, and subsequently present, a large fraction of body antigens. While the scope of promiscuously expressed genes by medullary thymic epithelial cells is well-established, relatively little is known about the expression of variants that are generated by co-transcriptional and post-transcriptional processes. RESULTS: Our study reveals that in comparison to other cell types, medullary thymic epithelial cells display significantly higher levels of alternative splicing, as well as A-to-I and C-to-U RNA editing, which thereby further expand the diversity of their self-antigen repertoire. Interestingly, Aire, the key mediator of promiscuous gene expression in these cells, plays a limited role in the regulation of these transcriptional processes. CONCLUSIONS: Our results highlight RNA processing as another layer by which the immune system assures a comprehensive self-representation in the thymus which is required for the establishment of self-tolerance and prevention of autoimmunity.
[Mh] Termos MeSH primário: Células Epiteliais/imunologia
Edição de RNA/genética
Timo/imunologia
[Mh] Termos MeSH secundário: Processamento Alternativo/genética
Processamento Alternativo/imunologia
Animais
Autoantígenos/genética
Autoantígenos/imunologia
Diferenciação Celular/imunologia
Regulação da Expressão Gênica/imunologia
Seres Humanos
Camundongos
Edição de RNA/imunologia
Tolerância a Antígenos Próprios/imunologia
Linfócitos T/imunologia
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Transcription Factors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:27777341
[Au] Autor:Hu CJ; Pan JB; Song G; Wen XT; Wu ZY; Chen S; Mo WX; Zhang FC; Qian J; Zhu H; Li YZ
[Ad] Endereço:From the ‡Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, Beijing, China100730.
[Ti] Título:Identification of Novel Biomarkers for Behcet Disease Diagnosis Using Human Proteome Microarray Approach.
[So] Source:Mol Cell Proteomics;16(2):147-156, 2017 Feb.
[Is] ISSN:1535-9484
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Behcet disease (BD) is a chronic systemic vasculitis and considered as an autoimmune disease. Although rare, BD can be fatal due to ruptured vascular aneurysms or severe neurological complications. To date, no known biomarker has been reported for this disease, making it difficult to diagnosis in the clinics. To undertake this challenge, we employed the HuProt arrays, each comprised of ∼20,000 unique human proteins, to identify BD-specific autoantibodies using a Two-Phase strategy established previously. In Phase I, we profiled the autoimmunity on the HuProt arrays with 75 serum samples collected from 40 BD patients, 15 diagnosed autoimmune patients who suffer from Takayasu arteritis (TA; n = 5)), ANCA associated vasculitis (AAV; n = 5), and Sjogren's syndrome (SS; n = 5), and 20 healthy subjects, and identified 20 candidate autoantigens that were significantly associated with BD. To validate these candidates, in Phase II we constructed a focused array with these 20 candidate BD-associated antigens, and use it to profile a much larger cohort, comprised of serum samples collected from 130 BD patients, 103 autoimmune patients (i.e. 40TA, 40 AAV and 23 SS), and 110 healthy controls. This allowed us to validate CTDP1 (RNA polymerase II subunit A C-terminal domain phosphatase)as a BD-specific autoantigen. The association of anti-CTDP1 with BD patients was further validated using the traditional Western blotting analysis. In conclusion, anti-CTDP1 antibody serves a novel autoantibody for Behcet disease and is expected to help more accurate clinical diagnosis.
[Mh] Termos MeSH primário: Síndrome de Behçet/diagnóstico
Fosfoproteínas Fosfatases/metabolismo
Análise Serial de Proteínas/métodos
Proteômica/métodos
[Mh] Termos MeSH secundário: Adulto
Autoanticorpos/imunologia
Autoantígenos/metabolismo
Síndrome de Behçet/imunologia
Biomarcadores/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Autoantigens); 0 (Biomarkers); EC 3.1.3.16 (Phosphoprotein Phosphatases); EC 3.1.3.16 (carboxy-terminal domain phosphatase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1074/mcp.M116.061002


  9 / 17960 MEDLINE  
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[PMID]:29272267
[Au] Autor:Peng Y
[Ad] Endereço:Division of Rheumatology, Department of Medicine, University of Washington, Seattle, Washington, United States of America.
[Ti] Título:Forced expression of IL-7R promotes CD8 T cell cytotoxicity to self antigen.
[So] Source:PLoS One;12(12):e0188112, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cross-presentation of apoptotic cell associated antigens by immature dendritic cells prevents the activation of self reactive CD8 T cells. Tolerized self reactive CD8 T cells down-regulate IL-7R expression on their surface. Whether over-expression of IL-7R can reverse their fate and function has not been examined. In this paper, we showed forced expression of IL-7R in OT-I T cells by a transgene enhanced CD8 T cell mediated diabetes in the RIP-mOVA model. Although IL-7R Tg (transgenic) did not completely reverse the deletion of OT-I T cells, it provided a significant survival advantage over w.t OT-I T cells. Furthermore, IL7R Tg OT-I T cells isolated from diabetic pancreata displayed increased production of IFN-γ, higher expression of T-bet, and increased externalization of CD107a. We also found that immature DCs containing apoptotic cells expressed high levels of PDL-1 on their surface. Although IL-7R Tg did not change PD1 expression on activated OT-I cells in vivo, the transgene enabled a significantly lower number of OT-I T cells to induce diabetes in the absence of PDL-1. Our results demonstrated that forced expression of IL-7R not only improved the functionality of tolerized CD8 T cells, it also acted in synergy with PDL-1 deficiency to further promote CD8 T cell cytotoxicity to self antigens.
[Mh] Termos MeSH primário: Autoantígenos/imunologia
Linfócitos T CD8-Positivos/imunologia
Receptores de Interleucina-7/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Apoptose
Anergia Clonal
Regulação para Baixo
Regulação da Expressão Gênica
Interferon gama/biossíntese
Camundongos
Camundongos Transgênicos
Ovalbumina/imunologia
Receptores de Interleucina-7/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Receptors, Interleukin-7); 82115-62-6 (Interferon-gamma); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188112


  10 / 17960 MEDLINE  
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[PMID]:27773721
[Au] Autor:Tajerian M; Hung V; Khan H; Lahey LJ; Sun Y; Birklein F; Krämer HH; Robinson WH; Kingery WS; Clark JD
[Ad] Endereço:Veterans Affairs Palo Alto Health Care System Palo Alto, CA, USA; Department of Anesthesiology, Stanford University School of Medicine, Stanford, CA, USA; Palo Alto Veterans Institute for Research, Palo Alto, CA, USA. Electronic address: maral@stanford.edu.
[Ti] Título:Identification of KRT16 as a target of an autoantibody response in complex regional pain syndrome.
[So] Source:Exp Neurol;287(Pt 1):14-20, 2017 Jan.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Using a mouse model of complex regional pain syndrome (CRPS), our goal was to identify autoantigens in the skin of the affected limb. METHODS: A CRPS-like state was induced using the tibia fracture/cast immobilization model. Three weeks after fracture, hindpaw skin was homogenized, run on 2-d gels, and probed by sera from fracture and control mice. Spots of interest were analyzed by liquid chromatography-mass spectroscopy (LC-MS) and the list of targets validated by examining their abundance and subcellular localization. In order to measure the autoantigenicity of selected protein targets, we quantified the binding of IgM in control and fracture mice sera, as well as in control and CRPS human sera, to the recombinant protein. RESULTS: We show unique binding between fracture skin extracts and fracture sera, suggesting the presence of auto-antigens. LC-MS analysis provided us a list of potential targets, some of which were upregulated after fracture (KRT16, eEF1a1, and PRPH), while others showed subcellular-redistribution and increased membrane localization (ANXA2 and ENO3). No changes in protein citrullination or carbamylation were observed. In addition to increased abundance, KRT16 demonstrated autoantigenicity, since sera from both fracture mice and CRPS patients showed increased autoantibody binding to recombinant kRT16 protein. CONCLUSIONS: Pursuing autoimmune contributions to CRPS provides a novel approach to understanding the condition and may allow the development of mechanism-based therapies. The identification of autoantibodies against KRT16 as a biomarker in mice and in humans is a critical step towards these goals, and towards redefining CRPS as having an autoimmune etiology.
[Mh] Termos MeSH primário: Autoantígenos/metabolismo
Síndromes da Dor Regional Complexa/sangue
Síndromes da Dor Regional Complexa/patologia
Queratina-6/imunologia
Queratina-6/metabolismo
Pele/metabolismo
Pele/ultraestrutura
Regulação para Cima/fisiologia
[Mh] Termos MeSH secundário: Adulto
Animais
Anexina A2/metabolismo
Autoantígenos/genética
Modelos Animais de Doenças
Membro Posterior/inervação
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Meia-Idade
Fator 1 de Elongação de Peptídeos/metabolismo
Periferinas/metabolismo
Fosfopiruvato Hidratase/metabolismo
Frações Subcelulares/metabolismo
Fraturas da Tíbia/sangue
Fraturas da Tíbia/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANXA2 protein, human); 0 (Annexin A2); 0 (Autoantigens); 0 (EEF1A1 protein, human); 0 (KRT6A protein, human); 0 (Keratin-6); 0 (PRPH protein, human); 0 (Peptide Elongation Factor 1); 0 (Peripherins); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161028
[St] Status:MEDLINE



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