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Pesquisa : A11.118.637.555.567.562.800 [Categoria DeCS]
Referências encontradas : 704 [refinar]
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[PMID]:28463873
[Au] Autor:Hu Y; Yoshida T; Georgopoulos K
[Ad] Endereço:Cutaneous Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA.
[Ti] Título:Transcriptional circuits in B cell transformation.
[So] Source:Curr Opin Hematol;24(4):345-352, 2017 Jul.
[Is] ISSN:1531-7048
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Loss of IKAROS in committed B cell precursors causes a block in differentiation while at the same time augments aberrant cellular properties, such as bone marrow stromal adhesion, self-renewal and resistance to glucocorticoid-mediated cell death. B cell acute lymphoblastic leukaemias originating from these early stages of B cell differentiation and associated with IKAROS mutations share a high-risk cellular phenotype suggesting that deregulation of IKAROS-based mechanisms cause a highly malignant disease process. RECENT STUDIES: Recent studies show that IKAROS is critical for the activity of super-enhancers at genes required for pre-B cell receptor (BCR) signalling and differentiation, working either downstream of or in parallel with B cell master regulators such as EBF1 and PAX5. IKAROS also directly represses a cryptic regulatory network of transcription factors prevalent in mesenchymal and epithelial precursors that includes YAP1, TEAD1/2, LHX2 and LMO2, and their targets, which are not normally expressed in lymphocytes. IKAROS prevents not only expression of these 'extra-lineage' transcription factors but also their cooperation with endogenous B cell master regulators, such as EBF1 and PAX5, leading to the formation of a de novo for lymphocytes super-enhancer network. IKAROS coordinates with the Polycomb repression complex (PRC2) to provide stable repression of associated genes during B cell development. However, induction of regulatory factors normally repressed by IKAROS starts a feed-forward loop that activates de-novo enhancers and elevates them to super-enhancer status, thereby diminishing PRC2 repression and awakening aberrant epithelial-like cell properties in B cell precursors. SUMMARY: Insight into IKAROS-based transcriptional circuits not only sets new paradigms for cell differentiation but also provides new approaches for classifying and treating high-risk human B-ALL that originates from these early stages of B cell differentiation.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Transformação Celular Neoplásica/genética
Regulação da Expressão Gênica
Redes Reguladoras de Genes
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Linfócitos B/patologia
Diferenciação Celular/genética
Proliferação Celular/genética
Autorrenovação Celular/genética
Elementos Facilitadores Genéticos
Seres Humanos
Fator de Transcrição Ikaros/metabolismo
Proteínas do Grupo Polycomb/metabolismo
Células Precursoras de Linfócitos B/citologia
Células Precursoras de Linfócitos B/metabolismo
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Polycomb-Group Proteins); 148971-36-2 (Ikaros Transcription Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1097/MOH.0000000000000352


  2 / 704 MEDLINE  
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[PMID]:27776452
[Au] Autor:Vo Ngoc DT; Krist L; van Overveld FJ; Rijkers GT
[Ad] Endereço:a Department of Science , University College Roosevelt , Middelburg , The Netherlands.
[Ti] Título:The long and winding road to IgA deficiency: causes and consequences.
[So] Source:Expert Rev Clin Immunol;13(4):371-382, 2017 04.
[Is] ISSN:1744-8409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The most common humoral immunodeficiency is IgA deficiency. One of the first papers addressing the cellular and molecular mechanisms underlying IgA deficiency indicated that immature IgA-positive B-lymphocytes are present in these patients. This suggests that the genetic background for IgA is still intact and that class switching can take place. At this moment, it cannot be ruled out that genetic as well as environmental factors are involved. Areas covered: A clinical presentation, the biological functions of IgA, and the management of IgA deficiency are reviewed. In some IgA deficient patients, a relationship with a loss-of-function mutation in the TACI (transmembrane activator and calcium-modulating cyclophilin ligand interaction) gene has been found. Many other genes also have been associated. Gut microbiota are an important environmental trigger for IgA synthesis. Expert commentary: Expression of IgA deficiency is due to both genetic and environmental factors and a role for gut microbiota cannot be excluded.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Deficiência de IgA/imunologia
Imunidade nas Mucosas
Imunoglobulina A/metabolismo
Microbiota/imunologia
Células Precursoras de Linfócitos B/fisiologia
Proteína Transmembrana Ativadora e Interagente do CAML/genética
[Mh] Termos MeSH secundário: Animais
Fator Ativador de Células B/genética
Interação Gene-Ambiente
Predisposição Genética para Doença
Seres Humanos
Deficiência de IgA/etiologia
Switching de Imunoglobulina
Polimorfismo Genético
Membro 13 da Superfamília de Ligantes de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (Immunoglobulin A); 0 (TNFRSF13B protein, human); 0 (Transmembrane Activator and CAML Interactor Protein); 0 (Tumor Necrosis Factor Ligand Superfamily Member 13)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1080/1744666X.2017.1248410


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[PMID]:29191653
[Au] Autor:Sun L; Kono N; Shimizu T; Toh H; Xue H; Numata O; Ato M; Itamura S; Ohnishi K
[Ad] Endereço:Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8572, Japan; Department of Immunology, National Institute of Infectious Diseases, Shinjuku, Tokyo 162-8640, Japan.
[Ti] Título:Distorted antibody repertoire developed in the absence of pre-B cell receptor formation.
[So] Source:Biochem Biophys Res Commun;495(1):1411-1417, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pre-B cell receptor (pre-BCR), consisting of the µ heavy chain (µHC) and the surrogate light chain (SLC, Vpre-B and λ5), plays important roles during B cell development. The formation of the pre-BCR, which enables the nascent immunoglobulin HC to associate with the SLC, is considered a prerequisite for B cell development. However, a significant number of peripheral mature (leaky) B cells exist in SLC-deficient mice. These leaky B cells develop in the absence of pre-BCR and do not undergo the pre-BCR checkpoint. The antibody repertoires of leaky B cells thus reflect the absence of pre-BCR function. To investigate how the absence of the pre-BCR is circumvented by these leaky-B cells and examine the effect of the pre-BCR checkpoint on the antibody system, we analyzed the antibody repertoires of λ5-deficient (λ5 ) mice using next-generation sequencing. In λ5 mice, spleen B cells displayed different patterns of VDJ-usage, relative to those in wild-type (WT) mice. Moreover, leaky B cells were neither derived from unusual B2 cells, characterized by particular LC gene rearrangements in the absence of pre-BCR signaling, nor from B1 cells, originating from different B cell progenitors. Analysis of the CDR-H3 amino acid sequences of µ-chain repertoires revealed that certain bone marrow B cells with particular CDR-H3 profiles undergo clonal expansion in λ5 mice. Part of these CDR-H3s contain arginine(s) in the middle of the CDR-H3 loop in λ5 mice, whereas few arginine(s) exist in this middle loop in WT CDR-H3s in the absence of clonal expansion. This CDR-H3 feature in λ5 mice presumably reflects the role of the pre-BCR in autoantibody regulation, since arginine(s) are often found in the antigen-binding site of autoantibodies. Here, we present a unique viewpoint on the role of pre-BCR, by assessing the whole antibody repertoire formed in SLC-deficient mice.
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Linfócitos B/citologia
Linfócitos B/imunologia
Receptores de Células Precursoras de Linfócitos B/imunologia
Células Precursoras de Linfócitos B/citologia
Células Precursoras de Linfócitos B/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/imunologia
Células Cultivadas
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Pre-B Cell Receptors)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:29262350
[Au] Autor:Suan D; Kräutler NJ; Maag JLV; Butt D; Bourne K; Hermes JR; Avery DT; Young C; Statham A; Elliott M; Dinger ME; Basten A; Tangye SG; Brink R
[Ad] Endereço:Immunology Division, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia; Westmead Clinical School, University of Sydney, Sydney, NSW 2145, Australia.
[Ti] Título:CCR6 Defines Memory B Cell Precursors in Mouse and Human Germinal Centers, Revealing Light-Zone Location and Predominant Low Antigen Affinity.
[So] Source:Immunity;47(6):1142-1153.e4, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Memory B cells (MBCs) and plasma cells (PCs) constitute the two cellular outputs of germinal center (GC) responses that together facilitate long-term humoral immunity. Although expression of the transcription factor BLIMP-1 identifies cells undergoing PC differentiation, no such marker exists for cells committed to the MBC lineage. Here, we report that the chemokine receptor CCR6 uniquely marks MBC precursors in both mouse and human GCs. CCR6 GC B cells were highly enriched within the GC light zone (LZ), were the most quiescent of all GC B cells, exhibited a cell-surface phenotype and gene expression signature indicative of an MBC transition, and possessed the augmented response characteristics of MBCs. MBC precursors within the GC LZ predominantly possessed a low affinity for antigen but also included cells from within the high-affinity pool. These data indicate a fundamental dichotomy between the processes that drive MBC and PC differentiation during GC responses.
[Mh] Termos MeSH primário: Centro Germinativo/imunologia
Imunidade Humoral
Plasmócitos/imunologia
Células Precursoras de Linfócitos B/imunologia
Receptores CCR6/imunologia
[Mh] Termos MeSH secundário: Animais
Antígeno B7-2/genética
Antígeno B7-2/imunologia
Diferenciação Celular
Linhagem da Célula/imunologia
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Centro Germinativo/citologia
Seres Humanos
Memória Imunológica
Imunofenotipagem
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fenótipo
Plasmócitos/citologia
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/imunologia
Células Precursoras de Linfócitos B/citologia
Receptores CCR6/genética
Receptores CXCR4/genética
Receptores CXCR4/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-2 Antigen); 0 (CCR6 protein, mouse); 0 (CXCR4 protein, mouse); 0 (Cd86 protein, mouse); 0 (Prdm1 protein, mouse); 0 (Receptors, CCR6); 0 (Receptors, CXCR4); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28991910
[Au] Autor:Syrett CM; Sindhava V; Hodawadekar S; Myles A; Liang G; Zhang Y; Nandi S; Cancro M; Atchison M; Anguera MC
[Ad] Endereço:Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia PA, United States of America.
[Ti] Título:Loss of Xist RNA from the inactive X during B cell development is restored in a dynamic YY1-dependent two-step process in activated B cells.
[So] Source:PLoS Genet;13(10):e1007050, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:X-chromosome inactivation (XCI) in female lymphocytes is uniquely regulated, as the inactive X (Xi) chromosome lacks localized Xist RNA and heterochromatin modifications. Epigenetic profiling reveals that Xist RNA is lost from the Xi at the pro-B cell stage and that additional heterochromatic modifications are gradually lost during B cell development. Activation of mature B cells restores Xist RNA and heterochromatin to the Xi in a dynamic two-step process that differs in timing and pattern, depending on the method of B cell stimulation. Finally, we find that DNA binding domain of YY1 is necessary for XCI in activated B cells, as ex-vivo YY1 deletion results in loss of Xi heterochromatin marks and up-regulation of X-linked genes. Ectopic expression of the YY1 zinc finger domain is sufficient to restore Xist RNA localization during B cell activation. Together, our results indicate that Xist RNA localization is critical for maintaining XCI in female lymphocytes, and that chromatin changes on the Xi during B cell development and the dynamic nature of YY1-dependent XCI maintenance in mature B cells predisposes X-linked immunity genes to reactivation.
[Mh] Termos MeSH primário: Inativação Gênica
Ativação Linfocitária/genética
Células Precursoras de Linfócitos B/metabolismo
RNA Longo não Codificante/genética
Inativação do Cromossomo X/genética
Fator de Transcrição YY1/metabolismo
[Mh] Termos MeSH secundário: Animais
Epigênese Genética
Feminino
Deleção de Genes
Genes Ligados ao Cromossomo X
Heterocromatina/genética
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
RNA Longo não Codificante/isolamento & purificação
Análise de Sequência de RNA
Baço/citologia
Regulação para Cima
Cromossomo X/genética
Fator de Transcrição YY1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heterochromatin); 0 (RNA, Long Noncoding); 0 (XIST non-coding RNA); 0 (YY1 Transcription Factor); 0 (Yy1 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007050


  6 / 704 MEDLINE  
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[PMID]:28957409
[Au] Autor:Moreau JM; Cen S; Berger A; Furlonger C; Paige CJ
[Ad] Endereço:Princess Margaret Cancer Centre, University Health Network, Toronto, Canada.
[Ti] Título:Bone marrow basophils provide survival signals to immature B cells in vitro but are dispensable in vivo.
[So] Source:PLoS One;12(9):e0185509, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immature B cells are the first B cell progenitors to express a fully formed B cell receptor and are therefore subject to extensive selection processes that act to mitigate the emergence of autoreactive clones. While it is well appreciated that most B cell generation in the bone marrow is highly dependent on access to molecules present in the local milieu, the existence of extrinsically provided factors that modulate immature B cell biology is ambiguous. Nonetheless, a population of CD49b+CD90lo cells has demonstrated in vitro potential to promote immature B cell survival. Using a mouse basophil reporter strain we confirmed the identity of these CD49b+CD90lo supportive cells as basophils. However, analysis of bone marrow B cell populations following lineage specific basophil depletion demonstrates that basophils do not have a significant role in vivo in modulating immature B cell biology during steady-state conditions.
[Mh] Termos MeSH primário: Basófilos/citologia
Células da Medula Óssea/citologia
Células Precursoras de Linfócitos B/citologia
[Mh] Termos MeSH secundário: Animais
Basófilos/metabolismo
Células da Medula Óssea/metabolismo
Linhagem da Célula
Sobrevivência Celular
Técnicas de Cocultura
Citoproteção
Feminino
Proteínas de Homeodomínio/metabolismo
Cadeias lambda de Imunoglobulina/metabolismo
Integrina alfa2/metabolismo
Contagem de Linfócitos
Camundongos
Células Precursoras de Linfócitos B/metabolismo
Antígenos Thy-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Immunoglobulin lambda-Chains); 0 (Integrin alpha2); 0 (Thy-1 Antigens); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185509


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[PMID]:28904124
[Au] Autor:Hamilton JA; Wu Q; Yang P; Luo B; Liu S; Hong H; Li J; Walter MR; Fish EN; Hsu HC; Mountz JD
[Ad] Endereço:Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294.
[Ti] Título:Cutting Edge: Endogenous IFN-ß Regulates Survival and Development of Transitional B Cells.
[So] Source:J Immunol;199(8):2618-2623, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transitional stage of B cell development is a formative stage in the spleen where autoreactive specificities are censored as B cells gain immune competence, but the intrinsic and extrinsic factors regulating survival of transitional stage 1 (T1) B cells are unknown. We report that B cell expression of IFN-ß is required for optimal survival and TLR7 responses of transitional B cells in the spleen and was overexpressed in T1 B cells from BXD2 lupus-prone mice. Single-cell gene expression analysis of B6 versus B6 T1 B cells revealed heterogeneous expression of in wild-type B cells and distinct gene expression patterns associated with endogenous IFN-ß. Single-cell analysis of BXD2 T1 B cells revealed that is expressed in early T1 B cell development with subsequent upregulation of and Together, these data suggest that T1 B cell expression of IFN-ß plays a key role in regulating responsiveness to external factors.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Interferon beta/metabolismo
Nefrite Lúpica/imunologia
Células Precursoras de Linfócitos B/imunologia
Baço/imunologia
[Mh] Termos MeSH secundário: Animais
Subpopulações de Linfócitos B/imunologia
Diferenciação Celular
Sobrevivência Celular
Suscetibilidade a Doenças
Interferon beta-1a/genética
Interferon beta-1a/metabolismo
Interferon-alfa
Ativação Linfocitária
Glicoproteínas de Membrana/genética
Glicoproteínas de Membrana/metabolismo
Camundongos
Camundongos Endogâmicos
Análise de Célula Única
Receptor 7 Toll-Like/genética
Receptor 7 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ifna1 protein, mouse); 0 (Interferon-alpha); 0 (Membrane Glycoproteins); 0 (Tlr7 protein, mouse); 0 (Toll-Like Receptor 7); 77238-31-4 (Interferon-beta); XRO4566Q4R (Interferon beta-1a)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700888


  8 / 704 MEDLINE  
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[PMID]:28807996
[Au] Autor:Bertocci B; Lecoeuche D; Sterlin D; Kühn J; Gaillard B; De Smet A; Lembo F; Bole-Feysot C; Cagnard N; Fadeev T; Dahan A; Weill JC; Reynaud CA
[Ad] Endereço:Équipe Développement du Systéme Immunitaire, Institut Necker-Enfant Malades, INSERM U1151-CNRS UMR8253, Faculté de Médecine Paris Decartes, Université Paris Descartes, Sorbone Paris Cité, 75993 Paris Cedex 14, France; barbara.bertocci@inserm.fr.
[Ti] Título:Klhl6 Deficiency Impairs Transitional B Cell Survival and Differentiation.
[So] Source:J Immunol;199(7):2408-2420, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Klhl6 belongs to the KLHL gene family, which is composed of an N-terminal BTB-POZ domain and four to six Kelch motifs in tandem. Several of these proteins function as adaptors of the Cullin3 E3 ubiquitin ligase complex. In this article, we report that Klhl6 deficiency induces, as previously described, a 2-fold reduction in mature B cells. However, we find that this deficit is centered on the inability of transitional type 1 B cells to survive and to progress toward the transitional type 2 B cell stage, whereas cells that have passed this step generate normal germinal centers (GCs) upon a T-dependent immune challenge. Klhl6-deficient type 1 B cells showed a 2-fold overexpression of genes linked with cell proliferation, including most targets of the anaphase-promoting complex/cyclosome complex, a set of genes whose expression is precisely downmodulated upon culture of splenic transitional B cells in the presence of BAFF. These results thus suggest a delay in the differentiation process of Klhl6-deficient B cells between the immature and transitional stage. We further show, in the BL2 Burkitt's lymphoma cell line, that KLHL6 interacts with Cullin3, but also that it binds to HBXIP/Lamtor5, a protein involved in cell-cycle regulation and cytokinesis. Finally, we report that KLHL6, which is recurrently mutated in B cell lymphomas, is an off-target of the normal somatic hypermutation process taking place in GC B cells in both mice and humans, thus leaving open whether, despite the lack of impact of Klhl6 deficiency on GC B cell expansion, mutants could contribute to the oncogenic process.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Proteínas de Transporte/fisiologia
Centro Germinativo/citologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Linfoma de Burkitt/patologia
Proteínas de Transporte/genética
Diferenciação Celular
Linhagem Celular
Proliferação Celular
Centro Germinativo/imunologia
Seres Humanos
Linfoma de Células B/genética
Linfoma de Células B/patologia
Camundongos
Mutação
Células Precursoras de Linfócitos B/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (KLHL6 protein, human); 0 (Klhl6 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700708


  9 / 704 MEDLINE  
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[PMID]:28739882
[Au] Autor:Liu X; Li YS; Shinton SA; Rhodes J; Tang L; Feng H; Jette CA; Look AT; Hayakawa K; Hardy RR
[Ad] Endereço:Fox Chase Cancer Center, Philadelphia, PA 19111.
[Ti] Título:Zebrafish B Cell Development without a Pre-B Cell Stage, Revealed by CD79 Fluorescence Reporter Transgenes.
[So] Source:J Immunol;199(5):1706-1715, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD79a and CD79b proteins associate with Ig receptors as integral signaling components of the B cell Ag receptor complex. To study B cell development in zebrafish, we isolated orthologs of these genes and performed in situ hybridization, finding that their expression colocalized with IgH-µ in the kidney, which is the site of B cell development. CD79 transgenic lines were made by linking the promoter and upstream regulatory segments of CD79a and CD79b to enhanced GFP to identify B cells, as demonstrated by PCR analysis of IgH-µ expression in sorted cells. We crossed these CD79-GFP lines to a recombination activating gene (Rag)2:mCherry transgenic line to identify B cell development stages in kidney marrow. Initiation of CD79:GFP expression in Rag2:mCherry cells and the timing of Ig H and L chain expression revealed simultaneous expression of both IgH-µ- and IgL-κ-chains, without progressing through the stage of IgH-µ-chain alone. Rag2:mCherry cells without CD79:GFP showed the highest Rag1 and Rag2 mRNAs compared with CD79a and CD79b:GFP B cells, which showed strongly reduced Rag mRNAs. Thus, B cell development in zebrafish does not go through a Rag CD79 IgH-µ pre-B cell stage, different from mammals. After the generation of CD79:GFP B cells, decreased CD79 expression occurred upon differentiation to Ig secretion, as detected by alteration from membrane to secreted IgH-µ exon usage, similar to in mammals. This confirmed a conserved role for CD79 in B cell development and differentiation, without the requirement of a pre-B cell stage in zebrafish.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Antígenos CD79/metabolismo
Proteínas de Peixes/metabolismo
Rim/fisiologia
Células Precursoras de Linfócitos B/fisiologia
Peixe-Zebra/imunologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Antígenos CD79/genética
Diferenciação Celular
Clonagem Molecular
Proteínas de Ligação a DNA/genética
Proteínas de Peixes/genética
Genes Reporter/genética
Proteínas de Fluorescência Verde/genética
Cadeias Pesadas de Imunoglobulinas/genética
Cadeias Pesadas de Imunoglobulinas/metabolismo
Cadeias Leves de Imunoglobulina/genética
Cadeias Leves de Imunoglobulina/metabolismo
Ativação Linfocitária
Transgenes/genética
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD79 Antigens); 0 (DNA-Binding Proteins); 0 (Fish Proteins); 0 (Immunoglobulin Heavy Chains); 0 (Immunoglobulin Light Chains); 0 (RAG2 protein, zebrafish); 0 (Zebrafish Proteins); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700552


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[PMID]:28735867
[Au] Autor:Lokau J; Flynn CM; Garbers C
[Ad] Endereço:Institute of Biochemistry, Kiel University, 24118 Kiel, Germany.
[Ti] Título:Cleavage of the Interleukin-11 receptor induces processing of its C-terminal fragments by the gamma-secretase and the proteasome.
[So] Source:Biochem Biophys Res Commun;491(2):296-302, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cytokine Interleukin-11 (IL-11) signals through the membrane-bound IL-11 receptor (IL-11R), which is expressed in a cell-type specific manner. We have recently shown that the metalloprotease ADAM10 can cleave the IL-11R. The liberated soluble IL-11R (sIL-11R) ectodomain can bind its ligand, and the resulting IL-11/sIL-11R complex can activate cells that do not express the IL-11R (trans-signaling). In this study, we show that the remaining C-terminal fragment (CTF1) after ADAM10-mediated cleavage is subsequently cleaved within the membrane by the gamma-secretase complex, and that the resulting shorter CTF2 is further degraded by the proteasome. In contrast to other transmembrane receptors, e.g. Notch, we find no evidence that the IL-11R CTF can translocate into the nucleus to act as a transcription factor, suggesting that regulated intramembrane proteolysis of the IL-11R CTF acts as a mechanism to clear the plasma membrane from remaining protein fragments after cleavage of its ectodomain.
[Mh] Termos MeSH primário: Proteína ADAM10/metabolismo
Secretases da Proteína Precursora do Amiloide/metabolismo
Interleucina-11/metabolismo
Proteínas de Membrana/metabolismo
Células Precursoras de Linfócitos B/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Receptores de Interleucina-11/metabolismo
[Mh] Termos MeSH secundário: Proteína ADAM10/genética
Proteína ADAM10/imunologia
Secretases da Proteína Precursora do Amiloide/genética
Secretases da Proteína Precursora do Amiloide/imunologia
Animais
Linhagem Celular Tumoral
Membrana Celular/imunologia
Membrana Celular/metabolismo
Expressão Gênica
Interleucina-11/genética
Interleucina-11/imunologia
Ligantes
Proteínas de Membrana/genética
Proteínas de Membrana/imunologia
Camundongos
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/imunologia
Fragmentos de Peptídeos/metabolismo
Células Precursoras de Linfócitos B/citologia
Células Precursoras de Linfócitos B/imunologia
Ligação Proteica
Proteólise
Receptores de Interleucina-11/genética
Receptores de Interleucina-11/imunologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-11); 0 (Ligands); 0 (Membrane Proteins); 0 (Peptide Fragments); 0 (Receptors, Interleukin-11); EC 3.4.- (Amyloid Precursor Protein Secretases); EC 3.4.24.81 (ADAM10 Protein); EC 3.4.24.81 (Adam10 protein, mouse); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE



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