Base de dados : MEDLINE
Pesquisa : G05.360.340.024.340.137.232.920 [Categoria DeCS]
Referências encontradas : 77 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 8 ir para página                    

  1 / 77 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29385200
[Au] Autor:Rout ED; Burnett RC; Labadie JD; Yoshimoto JA; Avery AC
[Ad] Endereço:Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, United States of America.
[Ti] Título:Preferential use of unmutated immunoglobulin heavy variable region genes in Boxer dogs with chronic lymphocytic leukemia.
[So] Source:PLoS One;13(1):e0191205, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human chronic lymphocytic leukemia (CLL) is a clinically heterogeneous disease, and immunoglobulin heavy variable region (IGHV) gene mutational status is an important prognostic marker. IGHV mutational status has not been previously examined in canine CLL. We sequenced the IGHV-D-J rearrangements from 55 canine patients with CLL, including 36 non-Boxer and 19 Boxer dogs. The majority of non-Boxers (75%) had mutated IGHV genes, whereas the majority of Boxers (79%) had unmutated IGHV genes. IGHV3-41 and IGHV3-67 gene usage was significantly higher in Boxers with CLL compared to non-Boxers. Additionally, 11 Boxers with large B-cell lymphoma and the normal IGHV repertoire of six control dogs (three Boxers and three non-Boxers) were sequenced. IGHV3-41 was preferentially used in Boxers with other forms of lymphoma and without lymphoproliferative disease. However, preferential use of unmutated IGHV genes was unique to Boxers with CLL, suggesting Boxers may be a valuable model to investigate unmutated CLL.
[Mh] Termos MeSH primário: Doenças do Cão/genética
Doenças do Cão/imunologia
Genes de Cadeia Pesada de Imunoglobulina
Região Variável de Imunoglobulina/genética
Leucemia Linfocítica Crônica de Células B/veterinária
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Estudos de Casos e Controles
Análise Mutacional de DNA
DNA de Neoplasias/genética
Cães
Feminino
Rearranjo Gênico de Cadeia Pesada de Linfócito B
Leucemia Linfocítica Crônica de Células B/genética
Leucemia Linfocítica Crônica de Células B/imunologia
Masculino
Mutação
Homologia de Sequência do Ácido Nucleico
Especificidade da Espécie
Éxons VDJ
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm); 0 (Immunoglobulin Variable Region)
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191205


  2 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28131552
[Au] Autor:Steiniger SC; Glanville J; Harris DW; Wilson TL; Ippolito GC; Dunham SA
[Ad] Endereço:Zoetis VMRD Global Therapeutics Research, 333 Portage Street, Kalamazoo, MI 49001, USA. Electronic address: sebastian.steiniger@zoetis.com.
[Ti] Título:Comparative analysis of the feline immunoglobulin repertoire.
[So] Source:Biologicals;46:81-87, 2017 Mar.
[Is] ISSN:1095-8320
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Next-Generation Sequencing combined with bioinformatics is a powerful tool for analyzing the large number of DNA sequences present in the expressed antibody repertoire and these data sets can be used to advance a number of research areas including antibody discovery and engineering. The accurate measurement of the immune repertoire sequence composition, diversity and abundance is important for understanding the repertoire response in infections, vaccinations and cancer immunology and could also be useful for elucidating novel molecular targets. In this study 4 individual domestic cats (Felis catus) were subjected to antibody repertoire sequencing with total number of sequences generated 1079863 for VH for IgG, 1050824 VH for IgM, 569518 for VK and 450195 for VL. Our analysis suggests that a similar VDJ expression patterns exists across all cats. Similar to the canine repertoire, the feline repertoire is dominated by a single subgroup, namely VH3. The antibody paratope of felines showed similar amino acid variation when compared to human, mouse and canine counterparts. All animals show a similarly skewed VH CDR-H3 profile and, when compared to canine, human and mouse, distinct differences are observed. Our study represents the first attempt to characterize sequence diversity in the expressed feline antibody repertoire and this demonstrates the utility of using NGS to elucidate entire antibody repertoires from individual animals. These data provide significant insight into understanding the feline immune system function.
[Mh] Termos MeSH primário: Variação Genética
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Cadeias Pesadas de Imunoglobulinas/genética
Cadeias Leves de Imunoglobulina/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Anticorpos/genética
Gatos
Regiões Determinantes de Complementaridade/genética
Cães
Perfilação da Expressão Gênica/métodos
Seres Humanos
Camundongos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Éxons VDJ/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Complementarity Determining Regions); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin Light Chains)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


  3 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27880974
[Au] Autor:Golding A; Darko S; Wylie WH; Douek DC; Shevach EM
[Ad] Endereço:Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
[Ti] Título:Deep sequencing of the TCR-ß repertoire of human forkhead box protein 3 (FoxP3) and FoxP3 T cells suggests that they are completely distinct and non-overlapping.
[So] Source:Clin Exp Immunol;188(1):12-21, 2017 Apr.
[Is] ISSN:1365-2249
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Maintenance of peripheral tolerance requires a balance between autoreactive conventional T cells (T ) and thymically derived forkhead box protein 3 (FoxP3) regulatory T cells (tT ). Considerable controversy exists regarding the similarities/differences in T cell receptor (TCR) repertoires expressed by T and tT . We generated highly purified populations of human adult and cord blood T and tT based on the differential expression of CD25 and CD127. The purity of the sorted populations was validated by intracellular staining for FoxP3 and Helios. We also purified an overlap group of CD4 T cells from adult donors to ensure that considerable numbers of shared clonotypes could be detected when present. We used deep sequencing of entire TCR-ß CDR3 sequences to analyse the TCR repertoire of T and tT . Our studies suggest that both neonatal and adult human T and tT cells are, in fact, entirely distinct CD4 T cell lineages.
[Mh] Termos MeSH primário: Fatores de Transcrição Forkhead/metabolismo
Sequenciamento de Nucleotídeos em Larga Escala
Fenótipo
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Subpopulações de Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Biomarcadores
Evolução Clonal
Regiões Determinantes de Complementaridade/genética
Seres Humanos
Imunofenotipagem
Receptores de Antígenos de Linfócitos T alfa-beta/metabolismo
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Éxons VDJ/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Complementarity Determining Regions); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Receptors, Antigen, T-Cell, alpha-beta)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161124
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12904


  4 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27574300
[Au] Autor:Meek K; Xu Y; Bailie C; Yu K; Neal JA
[Ad] Endereço:Department of Microbiology and Molecular Genetics, College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824; kmeek@msu.edu.
[Ti] Título:The ATM Kinase Restrains Joining of Both VDJ Signal and Coding Ends.
[So] Source:J Immunol;197(8):3165-3174, 2016 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The evidence that ATM affects resolution of RAG-induced DNA double-strand breaks is profuse and unequivocal; moreover, it is clear that the RAG complex itself cooperates (in an undetermined way) with ATM to facilitate repair of these double-strand breaks by the classical nonhomologous end-joining pathway. The mechanistic basis for the cooperation between ATM and the RAG complex has not been defined, although proposed models invoke ATM and RAG2's C terminus in maintaining the RAG postcleavage complex. In this study, we show that ATM reduces the rate of both coding and signal joining in a robust episomal assay; we suggest that this is the result of increased stability of the postcleavage complex. ATM's ability to inhibit VDJ joining requires its enzymatic activity. The noncore C termini of both RAG1 and RAG2 are also required for ATM's capacity to limit signal (but not coding) joining. Moreover, potential phosphorylation targets within the C terminus of RAG2 are also required for ATM's capacity to limit signal joining. These data suggest a model whereby the RAG signal end complex is stabilized by phosphorylation of RAG2 by ATM.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Proteínas de Ligação a DNA/metabolismo
Rearranjo Gênico do Linfócito B
Proteínas de Homeodomínio/metabolismo
Proteínas Nucleares/metabolismo
Éxons VDJ/genética
[Mh] Termos MeSH secundário: Proteínas Mutadas de Ataxia Telangiectasia/genética
Quebras de DNA de Cadeia Dupla
Proteínas de Ligação a DNA/genética
Células HEK293
Proteínas de Homeodomínio/genética
Seres Humanos
Complexos Multiproteicos/metabolismo
Proteínas Nucleares/genética
Fases de Leitura Aberta/genética
Fosforilação
Plasmídeos/genética
Sinais Direcionadores de Proteínas/genética
Estabilidade Proteica
Reparo de DNA por Recombinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Homeodomain Proteins); 0 (Multiprotein Complexes); 0 (Nuclear Proteins); 0 (Protein Sorting Signals); 0 (RAG2 protein, human); 128559-51-3 (RAG-1 protein); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE


  5 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26810227
[Au] Autor:Chen Z; Eder MD; Elos MT; Viboolsittiseri SS; Chen X; Wang JH
[Ad] Endereço:Department of Immunology and Microbiology, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045; and Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
[Ti] Título:Interplay between Target Sequences and Repair Pathways Determines Distinct Outcomes of AID-Initiated Lesions.
[So] Source:J Immunol;196(5):2335-47, 2016 Mar 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activation-induced deaminase (AID) functions by deaminating cytosines and causing U:G mismatches, a rate-limiting step of Ab gene diversification. However, precise mechanisms regulating AID deamination frequency remain incompletely understood. Moreover, it is not known whether different sequence contexts influence the preferential access of mismatch repair or uracil glycosylase (UNG) to AID-initiated U:G mismatches. In this study, we employed two knock-in models to directly compare the mutability of core Sµ and VDJ exon sequences and their ability to regulate AID deamination and subsequent repair process. We find that the switch (S) region is a much more efficient AID deamination target than the V region. Igh locus AID-initiated lesions are processed by error-free and error-prone repair. S region U:G mismatches are preferentially accessed by UNG, leading to more UNG-dependent deletions, enhanced by mismatch repair deficiency. V region mutation hotspots are largely determined by AID deamination. Recurrent and conserved S region motifs potentially function as spacers between AID deamination hotspots. We conclude that the pattern of mutation hotspots and DNA break generation is influenced by sequence-intrinsic properties, which regulate AID deamination and affect the preferential access of downstream repair. Our studies reveal an evolutionarily conserved role for substrate sequences in regulating Ab gene diversity and AID targeting specificity.
[Mh] Termos MeSH primário: Sítios de Ligação
Citidina Desaminase/metabolismo
Reparo do DNA
Motivos de Nucleotídeos
[Mh] Termos MeSH secundário: Alelos
Animais
Sequência de Bases
Reparo de Erro de Pareamento de DNA
Técnicas de Introdução de Genes
Ordem dos Genes
Marcação de Genes
Loci Gênicos
Camundongos
Camundongos Knockout
Proteína 2 Homóloga a MutS/metabolismo
Mutação
Taxa de Mutação
Especificidade por Substrato
Uracila-DNA Glicosidase/metabolismo
Éxons VDJ/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.2.2.- (Uracil-DNA Glycosidase); EC 3.5.4.- (AICDA (activation-induced cytidine deaminase)); EC 3.5.4.5 (Cytidine Deaminase); EC 3.6.1.3 (MutS Homolog 2 Protein)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160127
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1502184


  6 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26751373
[Au] Autor:Ralph DK; Matsen FA
[Ad] Endereço:Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
[Ti] Título:Consistency of VDJ Rearrangement and Substitution Parameters Enables Accurate B Cell Receptor Sequence Annotation.
[So] Source:PLoS Comput Biol;12(1):e1004409, 2016 Jan.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:VDJ rearrangement and somatic hypermutation work together to produce antibody-coding B cell receptor (BCR) sequences for a remarkable diversity of antigens. It is now possible to sequence these BCRs in high throughput; analysis of these sequences is bringing new insight into how antibodies develop, in particular for broadly-neutralizing antibodies against HIV and influenza. A fundamental step in such sequence analysis is to annotate each base as coming from a specific one of the V, D, or J genes, or from an N-addition (a.k.a. non-templated insertion). Previous work has used simple parametric distributions to model transitions from state to state in a hidden Markov model (HMM) of VDJ recombination, and assumed that mutations occur via the same process across sites. However, codon frame and other effects have been observed to violate these parametric assumptions for such coding sequences, suggesting that a non-parametric approach to modeling the recombination process could be useful. In our paper, we find that indeed large modern data sets suggest a model using parameter-rich per-allele categorical distributions for HMM transition probabilities and per-allele-per-position mutation probabilities, and that using such a model for inference leads to significantly improved results. We present an accurate and efficient BCR sequence annotation software package using a novel HMM "factorization" strategy. This package, called partis (https://github.com/psathyrella/partis/), is built on a new general-purpose HMM compiler that can perform efficient inference given a simple text description of an HMM.
[Mh] Termos MeSH primário: Biologia Computacional/métodos
Rearranjo Gênico do Linfócito B/genética
Anotação de Sequência Molecular/métodos
Éxons VDJ/genética
[Mh] Termos MeSH secundário: Simulação por Computador
Bases de Dados Genéticas
Seres Humanos
Modelos Genéticos
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170628
[Lr] Data última revisão:
170628
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1004409


  7 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26600245
[Au] Autor:Weinberger J; Jimenez-Heredia R; Schaller S; Suessner S; Sunzenauer J; Reindl-Schwaighofer R; Weiss R; Winkler S; Gabriel C; Danzer M; Oberbauer R
[Ad] Endereço:Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Linz, Austria.
[Ti] Título:Immune Repertoire Profiling Reveals that Clonally Expanded B and T Cells Infiltrating Diseased Human Kidneys Can Also Be Tracked in Blood.
[So] Source:PLoS One;10(11):e0143125, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent advances in high-throughput sequencing allow for the competitive analysis of the human B and T cell immune repertoire. In this study we compared Immunoglobulin and T cell receptor repertoires of lymphocytes found in kidney and blood samples of 10 patients with various renal diseases based on next-generation sequencing data. We used Biomed-2 primer panels and ImmunExplorer software to sequence, analyze and compare complementarity determining regions and V-(D)-J elements. While generally an individual's renal receptor repertoire is different from the repertoire present in blood, 94% (30/32) of the lymphocytes with clonal expansion in kidney can also be traced in blood however, not all of these clonotypes are equally abundant. Summarizing the data of all analyzed patients, 68% of highly expanded T cell clonotypes and 30% of the highly expanded B cell clonotypes that have infiltrated the kidney can be found amongst the five most abundant clonotypes in blood. In addition, complementarity determining region 3 sequences of the immunoglobulin heavy chains are on average more diverse than T cell receptor beta chains. Immune repertoire analysis of tissue infiltrating B and T cells adds new approaches to the assessment of adaptive immune response in kidney diseases. Our data suggest that expanded clonotypes in the tissues might be traceable in blood samples in the course of treatment or the natural history of the disease.
[Mh] Termos MeSH primário: Linfócitos B/patologia
Nefropatias/sangue
Nefropatias/imunologia
Rim/imunologia
Rim/patologia
Linfócitos T/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Sequência de Aminoácidos
Linfócitos B/imunologia
Proliferação Celular
Células Clonais
Regiões Determinantes de Complementaridade/química
Regiões Determinantes de Complementaridade/imunologia
Variação Genética
Seres Humanos
Meia-Idade
Dados de Sequência Molecular
Linfócitos T/imunologia
Éxons VDJ/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Complementarity Determining Regions)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0143125


  8 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26308889
[Au] Autor:Dong J; Panchakshari RA; Zhang T; Zhang Y; Hu J; Volpi SA; Meyers RM; Ho YJ; Du Z; Robbiani DF; Meng F; Gostissa M; Nussenzweig MC; Manis JP; Alt FW
[Ad] Endereço:Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
[Ti] Título:Orientation-specific joining of AID-initiated DNA breaks promotes antibody class switching.
[So] Source:Nature;525(7567):134-139, 2015 Sep 03.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During B-cell development, RAG endonuclease cleaves immunoglobulin heavy chain (IgH) V, D, and J gene segments and orchestrates their fusion as deletional events that assemble a V(D)J exon in the same transcriptional orientation as adjacent Cµ constant region exons. In mice, six additional sets of constant region exons (CHs) lie 100-200 kilobases downstream in the same transcriptional orientation as V(D)J and Cµ exons. Long repetitive switch (S) regions precede Cµ and downstream CHs. In mature B cells, class switch recombination (CSR) generates different antibody classes by replacing Cµ with a downstream CH (ref. 2). Activation-induced cytidine deaminase (AID) initiates CSR by promoting deamination lesions within Sµ and a downstream acceptor S region; these lesions are converted into DNA double-strand breaks (DSBs) by general DNA repair factors. Productive CSR must occur in a deletional orientation by joining the upstream end of an Sµ DSB to the downstream end of an acceptor S-region DSB. However, the relative frequency of deletional to inversional CSR junctions has not been measured. Thus, whether orientation-specific joining is a programmed mechanistic feature of CSR as it is for V(D)J recombination and, if so, how this is achieved is unknown. To address this question, we adapt high-throughput genome-wide translocation sequencing into a highly sensitive DSB end-joining assay and apply it to endogenous AID-initiated S-region DSBs in mouse B cells. We show that CSR is programmed to occur in a productive deletional orientation and does so via an unprecedented mechanism that involves in cis Igh organizational features in combination with frequent S-region DSBs initiated by AID. We further implicate ATM-dependent DSB-response factors in enforcing this mechanism and provide an explanation of why CSR is so reliant on the 53BP1 DSB-response factor.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Citidina Desaminase/metabolismo
Quebras de DNA de Cadeia Dupla
Reparo do DNA/genética
Switching de Imunoglobulina/genética
Regiões Constantes de Imunoglobulina/genética
Cadeias Pesadas de Imunoglobulinas/genética
[Mh] Termos MeSH secundário: Animais
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Linfócitos B/enzimologia
Linfócitos B/imunologia
Proteínas Cromossômicas não Histona/metabolismo
Proteínas de Ligação a DNA/metabolismo
Desaminação
Camundongos
Deleção de Sequência/genética
Proteína 1 de Ligação à Proteína Supressora de Tumor p53
Éxons VDJ/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromosomal Proteins, Non-Histone); 0 (DNA-Binding Proteins); 0 (Immunoglobulin Constant Regions); 0 (Immunoglobulin Heavy Chains); 0 (Trp53bp1 protein, mouse); 0 (Tumor Suppressor p53-Binding Protein 1); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 3.5.4.- (AICDA (activation-induced cytidine deaminase)); EC 3.5.4.5 (Cytidine Deaminase)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150827
[St] Status:MEDLINE
[do] DOI:10.1038/nature14970


  9 / 77 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26297338
[Au] Autor:Zhang W; Du Y; Su Z; Wang C; Zeng X; Zhang R; Hong X; Nie C; Wu J; Cao H; Xu X; Liu X
[Ad] Endereço:BGI-Shenzhen, Shenzhen 518083, China Shenzhen Key Laboratory of Transomics Biotechnologies, BGI-Shenzhen, Shenzhen 518083, China.
[Ti] Título:IMonitor: A Robust Pipeline for TCR and BCR Repertoire Analysis.
[So] Source:Genetics;201(2):459-72, 2015 Oct.
[Is] ISSN:1943-2631
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The advance of next generation sequencing (NGS) techniques provides an unprecedented opportunity to probe the enormous diversity of the immune repertoire by deep sequencing T-cell receptors (TCRs) and B-cell receptors (BCRs). However, an efficient and accurate analytical tool is still on demand to process the huge amount of data. We have developed a high-resolution analytical pipeline, Immune Monitor ("IMonitor") to tackle this task. This method utilizes realignment to identify V(D)J genes and alleles after common local alignment. We compare IMonitor with other published tools by simulated and public rearranged sequences, and it demonstrates its superior performance in most aspects. Together with this, a methodology is developed to correct the PCR and sequencing errors and to minimize the PCR bias among various rearranged sequences with different V and J gene families. IMonitor provides general adaptation for sequences from all receptor chains of different species and outputs useful statistics and visualizations. In the final part of this article, we demonstrate its application on minimal residual disease detection in patients with B-cell acute lymphoblastic leukemia. In summary, this package would be of widespread usage for immune repertoire analysis.
[Mh] Termos MeSH primário: Sequenciamento de Nucleotídeos em Larga Escala/métodos
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Receptores de Antígenos de Linfócitos B/genética
Receptores de Antígenos de Linfócitos T/genética
[Mh] Termos MeSH secundário: Alelos
Biologia Computacional
Seres Humanos
Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Éxons VDJ/genética
Éxons VDJ/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150823
[St] Status:MEDLINE
[do] DOI:10.1534/genetics.115.176735


  10 / 77 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26109644
[Au] Autor:Williams JM; Bonami RH; Hulbert C; Thomas JW
[Ad] Endereço:Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN 37232; and Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, TN 37232.
[Ti] Título:Reversing Tolerance in Isotype Switch-Competent Anti-Insulin B Lymphocytes.
[So] Source:J Immunol;195(3):853-64, 2015 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoreactive B lymphocytes that escape central tolerance and mature in the periphery are a liability for developing autoimmunity. IgG insulin autoantibodies that predict type 1 diabetes and complicate insulin therapies indicate that mechanisms for tolerance to insulin are flawed. To examine peripheral tolerance in anti-insulin B cells, we generated C57BL/6 mice that harbor anti-insulin VDJH-125 site directed to the native IgH locus (VH125(SD)). Class switch-competent anti-insulin B cells fail to produce IgG Abs following T cell-dependent immunization of VH125(SD) mice with heterologous insulin, and they exhibit markedly impaired proliferation to anti-CD40 plus insulin in vitro. In contrast, costimulation with LPS plus insulin drives robust anti-insulin B cell proliferation. Furthermore, VH125(SD) mice produce both IgM and IgG2a anti-insulin Abs following immunization with insulin conjugated to type 1 T cell-independent Brucella abortus ring test Ag (BRT). Anti-insulin B cells undergo clonal expansion in vivo and emerge as IgM(+) and IgM(-) GL7(+)Fas(+) germinal center (GC) B cells following immunization with insulin-BRT, but not BRT alone. Analysis of Igκ genes in VH125(SD) mice immunized with insulin-BRT reveals that anti-insulin Vκ from the preimmune repertoire is selected into GCs. These data demonstrate that class switch-competent anti-insulin B cells remain functionally silent in T cell-dependent immune responses, yet these B cells are vulnerable to reversal of anergy following combined BCR/TLR engagement that promotes Ag-specific GC responses and Ab production. Environmental factors that lead to infection and inflammation could play a critical yet underappreciated role in driving loss of tolerance and promoting autoimmune disease.
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Linfócitos B/imunologia
Diabetes Mellitus Tipo 1/imunologia
Anticorpos Anti-Insulina/imunologia
Insulina/imunologia
[Mh] Termos MeSH secundário: Animais
Autoanticorpos/biossíntese
Autoimunidade/imunologia
Antígenos CD40/imunologia
Diabetes Mellitus Tipo 1/genética
Tolerância Imunológica/imunologia
Imunoglobulina G/biossíntese
Imunoglobulina G/imunologia
Imunoglobulina M/biossíntese
Imunoglobulina M/imunologia
Lipopolissacarídeos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Dados de Sequência Molecular
Éxons VDJ/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantibodies); 0 (CD40 Antigens); 0 (Immunoglobulin G); 0 (Immunoglobulin M); 0 (Insulin); 0 (Insulin Antibodies); 0 (Lipopolysaccharides)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150626
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1403114



página 1 de 8 ir para página                    
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde