Base de dados : MEDLINE
Pesquisa : D02.172.045 [Categoria DeCS]
Referências encontradas : 370 [refinar]
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[PMID]:23008448
[Au] Autor:Aviszus K; Macleod MK; Kirchenbaum GA; Detanico TO; Heiser RA; St Clair JB; Guo W; Wysocki LJ
[Ad] Endereço:Integrated Department of Immunology, National Jewish Health and University of Colorado School of Medicine, Denver, CO 80206, USA.
[Ti] Título:Antigen-specific suppression of humoral immunity by anergic Ars/A1 B cells.
[So] Source:J Immunol;189(9):4275-83, 2012 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoreactive anergic B lymphocytes are considered to be dangerous because of their potential for activation and recruitment into autoimmune responses. However, they persist for days and constitute ∼5% of the B cell pool. We assessed their functional potential in the Ars/A1 transgene model, where anergic B cells express a dual-reactive Ag receptor that binds, in addition to a self-Ag, the hapten p-azophenylarsonate (Ars). When Ars/A1 B cells were transferred into adoptive recipients that were immunized with foreign proteins covalently conjugated with Ars, endogenous IgG immune responses to both were selectively and severely diminished, and the development of T helper cells was impaired. Approximately 95% inhibition of the anti-Ars response was attained with ∼4000 transferred Ars/A1 B cells through redundant mechanisms, one of which depended on their expression of MHC class II but not upon secretion of IL-10 or IgM. This Ag-specific suppressive activity implicates the autoreactive anergic B cell as an enforcer of immunological tolerance to self-Ags.
[Mh] Termos MeSH primário: Formação de Anticorpos
Subpopulações de Linfócitos B/imunologia
Subpopulações de Linfócitos B/metabolismo
Anergia Clonal/imunologia
Epitopos de Linfócito B/imunologia
Imunossupressão/métodos
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Autoantígenos/biossíntese
Autoantígenos/metabolismo
Subpopulações de Linfócitos B/transplante
Células Cultivadas
Epitopos de Linfócito B/metabolismo
Imunoglobulina G/biossíntese
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos A
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Tolerância a Antígenos Próprios/genética
Tolerância a Antígenos Próprios/imunologia
Baço/imunologia
Baço/metabolismo
Baço/transplante
p-Azobenzenoarsonato/biossíntese
p-Azobenzenoarsonato/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Autoantigens); 0 (Epitopes, B-Lymphocyte); 0 (Immunoglobulin G); 7334-23-8 (p-Azobenzenearsonate)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120926
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1201818


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[PMID]:19619554
[Au] Autor:Iglesias-Ussel MD; Zavadil J; Scharff MD
[Ad] Endereço:Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
[Ti] Título:Molecular characterization of hybridoma subclones spontaneously switching at high frequencies in vitro.
[So] Source:J Immunol Methods;350(1-2):71-8, 2009 Oct 31.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The hybridoma technology allows the production of large quantities of specific antibodies of a single isotype. Since different isotypes have special effector functions and are distributed distinctively throughout the body, it is often useful to have a library of switch variants from the original monoclonal antibody. We have shown previously that forced expression of activation induced cytidine deaminase (AID) in hybridomas increased their very low frequency of class switch recombination (CSR) in vitro only approximately 7-13 fold. Since we had previously identified rare hybridoma subclones that spontaneously switched at more than 100 times higher frequencies, we have now examined those higher switching variants to search for ways to further increase the frequency of isotype switching in vitro. AID was not responsible for the approximately 100 fold increase in CSR, so we used whole-genome gene expression profiling to provide a platform for studying candidate molecular pathways underlying spontaneous CSR in hybridomas.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Rearranjo Gênico do Linfócito B/imunologia
Hibridomas/imunologia
p-Azobenzenoarsonato/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/genética
Perfilação da Expressão Gênica/métodos
Regulação da Expressão Gênica/imunologia
Rearranjo Gênico do Linfócito B/genética
Camundongos
Análise de Sequência com Séries de Oligonucleotídeos/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 7334-23-8 (p-Azobenzenearsonate)
[Em] Mês de entrada:0911
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090722
[St] Status:MEDLINE
[do] DOI:10.1016/j.jim.2009.07.003


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[PMID]:17911603
[Au] Autor:Aviszus K; Zhang X; Wysocki LJ
[Ad] Endereço:Integrated Department of Immunology, National Jewish Medical and Research Center, University of Colorado School of Medicine, Denver, CO 80206, USA.
[Ti] Título:Silent development of memory progenitor B cells.
[So] Source:J Immunol;179(8):5181-90, 2007 Oct 15.
[Is] ISSN:0022-1767
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T cell-dependent immune responses generate long-lived plasma cells and memory B cells, both of which express hypermutated Ab genes. The relationship between these cell types is not entirely understood. Both appear to emanate from the germinal center reaction, but it is unclear whether memory cells evolve while obligatorily generating plasma cells by siblings under all circumstances. In the experiments we report, plasma cell development was functionally segregated from memory cell development by a series of closely spaced injections of Ag delivered during the period of germinal center development. The injection series elevated serum Ab of low affinity, supporting the idea that a strong Ag signal drives plasma cell development. At the same time, the injection series produced a distinct population of affinity/specificity matured memory B cells that were functionally silent, as manifested by an absence of corresponding serum Ab. These cells could be driven by a final booster injection to develop into Ab-forming cells. This recall response required that a rest period precede the final booster injection, but a pause of only 4 days was sufficient. Our results support a model of memory B cell development in which extensive affinity/specificity maturation can take place within a B cell clone under some circumstances in which a concomitant generation of Ab-forming cells by siblings does not take place.
[Mh] Termos MeSH primário: Subpopulações de Linfócitos B/citologia
Subpopulações de Linfócitos B/imunologia
Diferenciação Celular/imunologia
Memória Imunológica
Células Precursoras de Linfócitos B/citologia
Células Precursoras de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/biossíntese
Afinidade de Anticorpos
Especificidade de Anticorpos
Células Produtoras de Anticorpos/citologia
Células Produtoras de Anticorpos/imunologia
Células Produtoras de Anticorpos/metabolismo
Subpopulações de Linfócitos B/metabolismo
Haptenos/administração & dosagem
Haptenos/imunologia
Hemocianinas/administração & dosagem
Hemocianinas/imunologia
Hibridomas
Imunização Secundária
Camundongos
Camundongos Endogâmicos A
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Células Precursoras de Linfócitos B/metabolismo
p-Azobenzenoarsonato/administração & dosagem
p-Azobenzenoarsonato/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Haptens); 7334-23-8 (p-Azobenzenearsonate); 9013-72-3 (Hemocyanins); FV4Y0JO2CX (keyhole-limpet hemocyanin)
[Em] Mês de entrada:0711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:071004
[St] Status:MEDLINE


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[PMID]:14707052
[Au] Autor:Heltemes-Harris L; Liu X; Manser T
[Ad] Endereço:Kimmel Cancer Center and Department of Microbiology and Immunology, Jefferson Medical College, Philadelphia, PA 19107, USA.
[Ti] Título:Progressive surface B cell antigen receptor down-regulation accompanies efficient development of antinuclear antigen B cells to mature, follicular phenotype.
[So] Source:J Immunol;172(2):823-33, 2004 Jan 15.
[Is] ISSN:0022-1767
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have suggested that B cell Ag receptor (BCR) down-regulation by potentially pathological autoreactive B cells is associated with pathways leading to developmental arrest and receptor editing, or anergy. In this study we compare the primary development of B cells in two strains of mice expressing transgenic BCRs that differ by a single amino acid substitution that substantially increases reactivity for nuclear autoantigens such as DNA. Surprisingly, we find that both BCRs promote efficient development to mature follicular phenotype, but the strongly autoreactive BCR fails to promote marginal zone B cell development. The follicular B cells expressing the strongly autoreactive BCR do not appear to be anergic, as they robustly respond to polyclonal stimuli in vitro, are not short-lived, and can participate in germinal center reactions. Strikingly however, substantial and progressive down-modulation of surface IgM and IgD takes place throughout their primary development in the BM and periphery. We propose that BCR-autoantigen interactions regulate this pathway, resulting in reduced cellular avidity for autoantigens. This process of "learned ignorance" could allow autoreactive B cells access to the foreign Ag-driven memory B cell response, during which their self-reactivity would be attenuated by somatic hypermutation and selection in the germinal center.
[Mh] Termos MeSH primário: Autoantígenos/imunologia
Regulação para Baixo/imunologia
Imunofenotipagem
Receptores de Antígenos de Linfócitos B/antagonistas & inibidores
Receptores de Antígenos de Linfócitos B/biossíntese
[Mh] Termos MeSH secundário: Animais
Arginina/genética
Subpopulações de Linfócitos B/citologia
Subpopulações de Linfócitos B/imunologia
Subpopulações de Linfócitos B/metabolismo
Células da Medula Óssea/citologia
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Diferenciação Celular/genética
Diferenciação Celular/imunologia
Membrana Celular/genética
Membrana Celular/imunologia
Membrana Celular/metabolismo
Sobrevivência Celular/genética
Sobrevivência Celular/imunologia
Cadeias Pesadas de Imunoglobulinas/biossíntese
Cadeias Pesadas de Imunoglobulinas/genética
Cadeias Leves de Imunoglobulina/genética
Cadeias Leves de Imunoglobulina/metabolismo
Região Variável de Imunoglobulina/biossíntese
Região Variável de Imunoglobulina/genética
Camundongos
Camundongos Endogâmicos A
Camundongos Mutantes
Camundongos Transgênicos
Edição de RNA/imunologia
Receptores de Antígenos de Linfócitos B/genética
Receptores de Antígenos de Linfócitos B/imunologia
Baço/citologia
Baço/imunologia
Baço/metabolismo
p-Azobenzenoarsonato/imunologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Autoantigens); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin Light Chains); 0 (Immunoglobulin Variable Region); 0 (Receptors, Antigen, B-Cell); 7334-23-8 (p-Azobenzenearsonate); 94ZLA3W45F (Arginine)
[Em] Mês de entrada:0404
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:040107
[St] Status:MEDLINE


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[PMID]:12354384
[Au] Autor:Notidis E; Heltemes L; Manser T
[Ad] Endereço:Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.
[Ti] Título:Dominant, hierarchical induction of peripheral tolerance during foreign antigen-driven B cell development.
[So] Source:Immunity;17(3):317-27, 2002 Sep.
[Is] ISSN:1074-7613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We created mice expressing transgene-encoded BCRs with "dual reactivity" for the hapten Ars and nuclear autoantigens. Expression of transgene-encoded BCRs was not evident in the memory compartment despite observation of transgene-expressing B cells in germinal centers following Ars immunization. In contrast, dual reactive mAbs were readily obtained from mice with enforced expression of Bcl-2 following secondary Ars immunization. However, while these mAbs were hypermutated and displayed increased affinity for Ars, all had reduced avidity for DNA and intracellular autoantigens. Thus, Bcl-2 alters dominant-negative selection of dual reactive B cells during the Ars response, but this is restricted to those with lowered autoreactivity, demonstrating a hierarchy of peripheral tolerance during memory B cell development.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Tolerância Imunológica/imunologia
Memória Imunológica/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antinucleares/imunologia
Anticorpos Monoclonais/imunologia
Afinidade de Anticorpos
Especificidade de Anticorpos
Apoptose
Autoantígenos/imunologia
Autoimunidade/imunologia
Linfócitos B/citologia
Fusão Celular
Quimera
Cromatina/imunologia
Deleção Clonal
DNA/imunologia
Centro Germinativo/química
Centro Germinativo/imunologia
Haptenos/imunologia
Imunização
Cadeias Pesadas de Imunoglobulinas/imunologia
Região Variável de Imunoglobulina/imunologia
Isoantígenos/imunologia
Camundongos
Camundongos Endogâmicos A
Camundongos SCID
Camundongos Transgênicos
Mutação Puntual
Proteínas Proto-Oncogênicas c-bcl-2/biossíntese
Receptores de Antígenos de Linfócitos B/genética
Hipermutação Somática de Imunoglobulina
Transgenes
p-Azobenzenoarsonato/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Antibodies, Monoclonal); 0 (Autoantigens); 0 (Chromatin); 0 (Haptens); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin Variable Region); 0 (Isoantigens); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, Antigen, B-Cell); 7334-23-8 (p-Azobenzenearsonate); 9007-49-2 (DNA)
[Em] Mês de entrada:0211
[Cu] Atualização por classe:170211
[Lr] Data última revisão:
170211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:021002
[St] Status:MEDLINE


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[PMID]:11730840
[Au] Autor:Parhami-Seren B; Viswanathan M; Margolies MN
[Ad] Endereço:Department of Biochemistry, College of Medicine, University of Vermont, Burlington, VT 05405-0068, USA. bparhami@zoo.uvm.edu
[Ti] Título:Selection of high affinity p-azophenyarsonate Fabs from heavy-chain CDR2 insertion libraries.
[So] Source:J Immunol Methods;259(1-2):43-53, 2002 Jan 01.
[Is] ISSN:0022-1759
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The length of the heavy chain complementarity-determining region two (HCDR2) of the unmutated anti-p-azophenylarsonate (Ars) monoclonal antibody (36-65 mAb) was extended by three residues in order to test whether this insertion can provide additional contacts between the Ab and the antigen. Two libraries were generated using 36-65 heavy and light chain genes which were cloned as Fab in the phage-display vector pComb3. In the first library, three randomized amino acids were inserted between residues Gly 54 and Asn 55, which are the most solvent exposed residues in the HCDR2 loop. In the second library, in addition to the 3-mer randomized insertion, the flanking residues at positions 54 and 55 were also randomized to allow additional loop flexibility for binding to Ars. Solid-phase and solution phase affinity panning were used to select for clones that bind to Ars. Results indicate that diverse 3-mer HCDR2 insertions can be tolerated, and affinities 10-fold higher than germline encoded 36-65 Ab can be obtained. The sequence diversity of the insertion among the selected clones from both libraries suggests that the insertion increases contact between the Ab and the protein carrier rather than the hapten alone.
[Mh] Termos MeSH primário: Afinidade de Anticorpos/genética
Regiões Determinantes de Complementaridade/genética
Cadeias Pesadas de Imunoglobulinas/genética
[Mh] Termos MeSH secundário: Animais
Regiões Determinantes de Complementaridade/imunologia
Hibridomas
Fragmentos Fab das Imunoglobulinas/genética
Fragmentos Fab das Imunoglobulinas/imunologia
Cadeias Pesadas de Imunoglobulinas/imunologia
Camundongos
Mutagênese Insercional
Biblioteca de Peptídeos
Engenharia de Proteínas
p-Azobenzenoarsonato
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Complementarity Determining Regions); 0 (Immunoglobulin Fab Fragments); 0 (Immunoglobulin Heavy Chains); 0 (Peptide Library); 7334-23-8 (p-Azobenzenearsonate)
[Em] Mês de entrada:0202
[Cu] Atualização por classe:071114
[Lr] Data última revisão:
071114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:011204
[St] Status:MEDLINE


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[PMID]:11785672
[Au] Autor:Notidis E; Hande S; Manser T
[Ad] Endereço:Department of Microbiology and Immunology and The Kimmel Cancer Institute, Thomas Jefferson Medical College, Philadelphia, PA 19107, USA.
[Ti] Título:Enforced expression of Bcl-2 selectively perturbs negative selection of dual reactive antibodies.
[So] Source:Dev Immunol;8(3-4):223-34, 2001.
[Is] ISSN:1044-6672
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We investigated the role of apoptosis in the development of B cell memory by analyzing the (p-azophenylarsonate) Ars response in a line of A strain mice in which expression of human Bcl-2 was enforced in the B cell compartment. Previous studies of the Ars immune response in these A. Bcl-2 mice, demonstrated that a large percentage of the antibodies expressed by the Ars induced memory B cell compartment had accumulated point mutations via somatic hypermutation that increased their affinity for both Ars and the autoantigen DNA ("dual reactive" antibodies). This was in sharp contrast to normal A strain mice which displayed no dual reactive B cells in their Ars induced memory B cell compartment. These data suggested that interference with apoptotic pathways regulated by Bcl-2 allows developing memory B cells that have acquired autoreactivity to bypass a peripheral tolerance checkpoint. Further studies of these mice, reported here, demonstrate that enforced expression of Bcl-2 does not alter serum antibody affinity maturation nor positive selection of B cells expressing somatically mutated antibody with an increased affinity for Ars. Moreover, the somatic hypermutation process was unaffected in A. Bcl-2 mice. Thus, enforced expression of Bcl-2 in A. Bcl-2 mice appears to selectively alter a negative selection process that operates during memory B cell differentiation.
[Mh] Termos MeSH primário: Anticorpos/imunologia
Linfócitos B/imunologia
Deleção Clonal
Proteínas Proto-Oncogênicas c-bcl-2/fisiologia
p-Azobenzenoarsonato/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antinucleares/imunologia
Afinidade de Anticorpos
Autoimunidade
Sequência de Bases
DNA/imunologia
Expressão Gênica
Cadeias Pesadas de Imunoglobulinas/genética
Região Variável de Imunoglobulina/genética
Memória Imunológica
Camundongos
Camundongos Endogâmicos A
Camundongos Transgênicos
Dados de Sequência Molecular
Mutação
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Hipermutação Somática de Imunoglobulina
Baço/citologia
Baço/imunologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies); 0 (Antibodies, Antinuclear); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin Variable Region); 0 (Proto-Oncogene Proteins c-bcl-2); 7334-23-8 (p-Azobenzenearsonate); 9007-49-2 (DNA)
[Em] Mês de entrada:0208
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020112
[St] Status:MEDLINE


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[PMID]:11673524
[Au] Autor:Parhami-Seren B; Viswanathan M; Strong RK; Margolies MN
[Ad] Endereço:Department of Biochemistry, College of Medicine, University of Vermont, Burlington, VT 05405, USA. bparhami@zoo.uvm.edu
[Ti] Título:Structural analysis of mutants of high-affinity and low-affinity p-azophenylarsonate-specific antibodies generated by alanine scanning of heavy chain complementarity-determining region 2.
[So] Source:J Immunol;167(9):5129-35, 2001 Nov 01.
[Is] ISSN:0022-1767
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alanine scanning was used to determine the affinity contributions of 10 side chain amino acids (residues at position 50-60 inclusive) of H chain complementarity-determining region 2 (HCDR2) of the somatically mutated high-affinity anti-p-azophenylarsonate Ab, 36-71. Each mutated H chain gene was expressed in the context of mutated (36-71L) and the unmutated (36-65L) L chains to also assess the contribution of L chain mutations to affinity. Combined data from fluorescence quenching, direct binding, inhibition, and capture assays indicated that mutating H:Tyr(50) and H:Tyr(57) to Ala in the 36-71 H chain results in significant loss of binding with both mutated (36-71L) or unmutated (36-65L) L chain, although the decrease was more pronounced when unmutated L chain was used. All other HCDR2 mutations in 36-71 had minimal effect on Ab affinity when expressed with 36-71 L chain. However, in the context of unmutated L chain, of H:Gly(54) to Ala resulted in significant loss of binding, while Abs containing Asn(52) to Ala, Pro(53) to Ala, or Ile(58) to Ala mutation exhibited 4.3- to 7.1-fold reduced affinities. When alanine scanning was performed instead on certain HCDR2 residues of the germline-encoded (unmutated) 36-65 Ab and expressed with unmutated L chain as Fab in bacteria, these mutants exhibited affinities similar to or slightly higher than the wild-type 36-65. These findings indicate an important role of certain HCDR2 side chain residues on Ab affinity and the constraints imposed by L chain mutations in maintaining Ag binding.
[Mh] Termos MeSH primário: Anticorpos/química
Afinidade de Anticorpos
Regiões Determinantes de Complementaridade/química
Cadeias Pesadas de Imunoglobulinas/química
[Mh] Termos MeSH secundário: Alanina
Animais
Escherichia coli/genética
Camundongos
Mutagênese
p-Azobenzenoarsonato/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies); 0 (Complementarity Determining Regions); 0 (Immunoglobulin Heavy Chains); 7334-23-8 (p-Azobenzenearsonate); OF5P57N2ZX (Alanine)
[Em] Mês de entrada:0112
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:011024
[St] Status:MEDLINE


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[PMID]:11282987
[Au] Autor:Tumas-Brundage KM; Notidis E; Heltemes L; Zhang X; Wysocki LJ; Manser T
[Ad] Endereço:Department of Immunology, National Jewish Medical and Research Center and University of Colorado School of Medicine, Denver, CO 80262, USA.
[Ti] Título:Predominance of a novel splenic B cell population in mice expressing a transgene that encodes multireactive antibodies: support for additional heterogeneity of the B cell compartment.
[So] Source:Int Immunol;13(4):475-84, 2001 Apr.
[Is] ISSN:0953-8178
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We generated IgHmudelta transgenic mice using a V(H) gene that in A/J mice encodes multireactive BCR in the preimmune B cell compartment and is predominantly expressed by a memory B cell subpopulation. Most primary splenic B cells in these mice have a size, cell-surface phenotype and in vitro response profile distinct from mature follicular (B2), marginal zone (MZ) or B1 B cells, but are long-lived and appear to be slowly cycling. They reside in conventional B cell areas of the spleen and mount robust foreign antigen-driven germinal center responses, but do not efficiently differentiate to secretory phenotype. We propose that these qualities result from ongoing, low-avidity BCR-self-ligand interactions and promote entry into the memory pathway. Given these data, and the enormous diversity and characteristic multireactivity of the preimmune antibody repertoire, we also suggest that it may be more appropriate to view the primary B cell compartment as a continuum of functional and phenotypic 'layers', rather than as a group of discrete B1, B2 and MZ subsets.
[Mh] Termos MeSH primário: Anticorpos/genética
Linfócitos B/imunologia
Diferenciação Celular
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anticorpos/sangue
Antígenos de Diferenciação de Linfócitos B/análise
Linfócitos B/citologia
Tamanho Celular
Imunização
Cadeias Pesadas de Imunoglobulinas/genética
Imunoglobulinas/sangue
Linfonodos/imunologia
Camundongos
Camundongos Transgênicos
Receptores de Antígenos de Linfócitos B/análise
Baço/citologia
Baço/imunologia
p-Azobenzenoarsonato/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Antibodies); 0 (Antigens, Differentiation, B-Lymphocyte); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulins); 0 (Receptors, Antigen, B-Cell); 7334-23-8 (p-Azobenzenearsonate)
[Em] Mês de entrada:0106
[Cu] Atualização por classe:071114
[Lr] Data última revisão:
071114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:010403
[St] Status:MEDLINE


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[PMID]:11163228
[Au] Autor:Benschop RJ; Aviszus K; Zhang X; Manser T; Cambier JC; Wysocki LJ
[Ad] Endereço:Integrated Department of Immunology, National Jewish Medical and Research Center and, University of Colorado School of Medicine, Denver, CO 80206, USA.
[Ti] Título:Activation and anergy in bone marrow B cells of a novel immunoglobulin transgenic mouse that is both hapten specific and autoreactive.
[So] Source:Immunity;14(1):33-43, 2001 Jan.
[Is] ISSN:1074-7613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Available evidence indicates that B cell tolerance is attained by receptor editing, anergy, or clonal deletion. Here, we describe a p-azophenylarsonate (Ars)-specific immunoglobulin transgenic mouse in which B cells become anergic as a consequence of cross-reaction with autoantigen in the bone marrow. Developing bone marrow B cells show no evidence of receptor editing but transiently upregulate activation markers and appear to undergo accelerated development. Mature B cells are present in normal numbers but are refractory to BCR-mediated induction of calcium mobilization, tyrosine phosphorylation, and antibody responses. Activation marker expression and acquisition of the anergic phenotype is prevented in bone marrow cultures by monovalent hapten. In this model, it appears that induction of anergy in B cells can be prevented by monovalent hapten competing with autoantigen for the binding site.
[Mh] Termos MeSH primário: Autoimunidade/imunologia
Linfócitos B/imunologia
Células da Medula Óssea/imunologia
Anergia Clonal/imunologia
Haptenos/imunologia
Imunoglobulinas/imunologia
Ativação Linfocitária/imunologia
[Mh] Termos MeSH secundário: Alelos
Animais
Biomarcadores
DNA de Cadeia Simples/imunologia
Expressão Gênica
Hemocianinas/imunologia
Cadeias delta de Imunoglobulina/genética
Cadeias delta de Imunoglobulina/imunologia
Cadeias kappa de Imunoglobulina/genética
Cadeias kappa de Imunoglobulina/imunologia
Cadeias mu de Imunoglobulina/genética
Cadeias mu de Imunoglobulina/imunologia
Imunoglobulinas/genética
Camundongos
Camundongos Transgênicos
Transgenes
p-Azobenzenoarsonato/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Biomarkers); 0 (DNA, Single-Stranded); 0 (Haptens); 0 (Immunoglobulin delta-Chains); 0 (Immunoglobulin kappa-Chains); 0 (Immunoglobulin mu-Chains); 0 (Immunoglobulins); 7334-23-8 (p-Azobenzenearsonate); 9013-72-3 (Hemocyanins); FV4Y0JO2CX (keyhole-limpet hemocyanin)
[Em] Mês de entrada:0104
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:010213
[St] Status:MEDLINE



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