Base de dados : MEDLINE
Pesquisa : A11.148.378.294 [Categoria DeCS]
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[PMID]:29192121
[Au] Autor:Karlsson G; Sigvardsson M; Böiers C
[Ad] Endereço:Lund Stem Cell Center, Lund University, Lund, Sweden.
[Ti] Título:Don't judge a cell by its cover: heterogeneity within early lymphoid progenitors.
[So] Source:EMBO J;36(24):3552-3554, 2017 12 15.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Células-Tronco Hematopoéticas
Células Progenitoras Linfoides
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201798443


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[PMID]:29059182
[Au] Autor:Odhams CA; Cunninghame Graham DS; Vyse TJ
[Ad] Endereço:Department of Medical & Molecular Genetics, King's College London, London, United Kingdom.
[Ti] Título:Profiling RNA-Seq at multiple resolutions markedly increases the number of causal eQTLs in autoimmune disease.
[So] Source:PLoS Genet;13(10):e1007071, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genome-wide association studies have identified hundreds of risk loci for autoimmune disease, yet only a minority (~25%) share genetic effects with changes to gene expression (eQTLs) in immune cells. RNA-Seq based quantification at whole-gene resolution, where abundance is estimated by culminating expression of all transcripts or exons of the same gene, is likely to account for this observed lack of colocalisation as subtle isoform switches and expression variation in independent exons can be concealed. We performed integrative cis-eQTL analysis using association statistics from twenty autoimmune diseases (560 independent loci) and RNA-Seq data from 373 individuals of the Geuvadis cohort profiled at gene-, isoform-, exon-, junction-, and intron-level resolution in lymphoblastoid cell lines. After stringently testing for a shared causal variant using both the Joint Likelihood Mapping and Regulatory Trait Concordance frameworks, we found that gene-level quantification significantly underestimated the number of causal cis-eQTLs. Only 5.0-5.3% of loci were found to share a causal cis-eQTL at gene-level compared to 12.9-18.4% at exon-level and 9.6-10.5% at junction-level. More than a fifth of autoimmune loci shared an underlying causal variant in a single cell type by combining all five quantification types; a marked increase over current estimates of steady-state causal cis-eQTLs. Causal cis-eQTLs detected at different quantification types localised to discrete epigenetic annotations. We applied a linear mixed-effects model to distinguish cis-eQTLs modulating all expression elements of a gene from those where the signal is only evident in a subset of elements. Exon-level analysis detected disease-associated cis-eQTLs that subtly altered transcription globally across the target gene. We dissected in detail the genetic associations of systemic lupus erythematosus and functionally annotated the candidate genes. Many of the known and novel genes were concealed at gene-level (e.g. IKZF2, TYK2, LYST). Our findings are provided as a web resource.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica
Lúpus Eritematoso Sistêmico/genética
Locos de Características Quantitativas
[Mh] Termos MeSH secundário: Estudos de Casos e Controles
Linhagem Celular
Grupo com Ancestrais do Continente Europeu/genética
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Modelos Lineares
Células Progenitoras Linfoides/citologia
Polimorfismo de Nucleotídeo Único
Análise de Sequência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007071


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[PMID]:29045900
[Au] Autor:Alhaj Hussen K; Vu Manh TP; Guimiot F; Nelson E; Chabaane E; Delord M; Barbier M; Berthault C; Dulphy N; Alberdi AJ; Burlen-Defranoux O; Socié G; Bories JC; Larghero J; Vanneaux V; Verhoeyen E; Wirth T; Dalod M; Gluckman JC; Cumano A; Canque B
[Ad] Endereço:INSERM U1126, Université Paris-Diderot, École Pratique des Hautes Etudes/PSL Research University, Institut Universitaire d'Hématologie, Hôpital Saint-Louis, Paris, France.
[Ti] Título:Molecular and Functional Characterization of Lymphoid Progenitor Subsets Reveals a Bipartite Architecture of Human Lymphopoiesis.
[So] Source:Immunity;47(4):680-696.e8, 2017 Oct 17.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The classical model of hematopoiesis established in the mouse postulates that lymphoid cells originate from a founder population of common lymphoid progenitors. Here, using a modeling approach in humanized mice, we showed that human lymphoid development stemmed from distinct populations of CD127 and CD127 early lymphoid progenitors (ELPs). Combining molecular analyses with in vitro and in vivo functional assays, we demonstrated that CD127 and CD127 ELPs emerged independently from lympho-mono-dendritic progenitors, responded differently to Notch1 signals, underwent divergent modes of lineage restriction, and displayed both common and specific differentiation potentials. Whereas CD127 ELPs comprised precursors of T cells, marginal zone B cells, and natural killer (NK) and innate lymphoid cells (ILCs), CD127 ELPs supported production of all NK cell, ILC, and B cell populations but lacked T potential. On the basis of these results, we propose a "two-family" model of human lymphoid development that differs from the prevailing model of hematopoiesis.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Células Matadoras Naturais/metabolismo
Células Progenitoras Linfoides/metabolismo
Linfopoese/genética
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Linfócitos B/citologia
Diferenciação Celular/genética
Linhagem da Célula/genética
Células Cultivadas
Feminino
Perfilação da Expressão Gênica/métodos
Seres Humanos
Subunidade gama Comum de Receptores de Interleucina/deficiência
Subunidade gama Comum de Receptores de Interleucina/genética
Subunidade alfa de Receptor de Interleucina-7/genética
Subunidade alfa de Receptor de Interleucina-7/metabolismo
Células Matadoras Naturais/citologia
Células Progenitoras Linfoides/citologia
Células Progenitoras Linfoides/transplante
Masculino
Camundongos Endogâmicos NOD
Camundongos Knockout
Camundongos SCID
Meia-Idade
Transplante de Células-Tronco
Linfócitos T/citologia
Transplante Heterólogo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Il2rg protein, mouse); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-7 Receptor alpha Subunit)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE


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[PMID]:28931604
[Au] Autor:Xiao S; Shterev ID; Zhang W; Young L; Shieh JH; Moore M; van den Brink M; Sempowski GD; Manley NR
[Ad] Endereço:Department of Genetics, Paul D. Coverdell Center, University of Georgia, Athens, GA 30602; nmanley@uga.edu shiyun@uga.edu.
[Ti] Título:Sublethal Total Body Irradiation Causes Long-Term Deficits in Thymus Function by Reducing Lymphoid Progenitors.
[So] Source:J Immunol;199(8):2701-2712, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Total body irradiation (TBI) damages hematopoietic cells in the bone marrow and thymus; however, the long-term effects of irradiation with aging remain unclear. In this study, we found that the impact of radiation on thymopoiesis in mice varied by sex and dose but, overall, thymopoiesis remained suppressed for ≥12 mo after a single exposure. Male and female mice showed a long-term dose-dependent reduction in thymic cKit lymphoid progenitors that was maintained throughout life. Damage to hematopoietic stem cells (HSCs) in the bone marrow was dose dependent, with as little as 0.5 Gy causing a significant long-term reduction. In addition, the potential for T lineage commitment was radiation sensitive with aging. Overall, the impact of irradiation on the hematopoietic lineage was more severe in females. In contrast, the rate of decline in thymic epithelial cell numbers with age was radiation-sensitive only in males, and other characteristics including transcription were unaffected. Taken together, these data suggest that long-term suppression of thymopoiesis after sublethal irradiation was primarily due to fewer progenitors in the BM combined with reduced potential for T lineage commitment. A single irradiation dose also caused synchronization of thymopoiesis, with a periodic thymocyte differentiation profile persisting for at least 12 mo postirradiation. This study suggests that the number and capability of HSCs for T cell production can be dramatically and permanently damaged after a single relatively low TBI dose, accelerating aging-associated thymic involution. Our findings may impact evaluation and therapeutic intervention of human TBI events.
[Mh] Termos MeSH primário: Células da Medula Óssea/fisiologia
Hematopoese/efeitos da radiação
Síndromes de Imunodeficiência/imunologia
Células Progenitoras Linfoides/fisiologia
Linfócitos T/fisiologia
Timo/efeitos da radiação
[Mh] Termos MeSH secundário: Envelhecimento
Animais
Diferenciação Celular
Linhagem da Célula
Células Cultivadas
Feminino
Síndromes de Imunodeficiência/etiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Proto-Oncogênicas c-kit/metabolismo
Timo/imunologia
Irradiação Corporal Total/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[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:170922
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600934


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[PMID]:28825702
[Au] Autor:Berthault C; Ramond C; Burlen-Defranoux O; Soubigou G; Chea S; Golub R; Pereira P; Vieira P; Cumano A
[Ad] Endereço:Unit for Lymphopoiesis, Pasteur Institute, Paris, France. Immunology department.
[Ti] Título:Asynchronous lineage priming determines commitment to T cell and B cell lineages in fetal liver.
[So] Source:Nat Immunol;18(10):1139-1149, 2017 Oct.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The molecular events that initiate lymphoid-lineage specification remain unidentified because the stages of differentiation during which lineage commitment occurs are difficult to characterize. We isolated fetal liver progenitor cells undergoing restriction of their differentiation potential toward the T cell-innate lymphoid cell lineage or the B cell lineage. Transcripts that defined the molecular signatures of these two subsets were sequentially upregulated in lympho-myeloid precursor cells and in common lymphoid progenitor cells, respectively, and this preceded lineage restriction; this indicates that T cell-versus-B cell commitment is not a binary fate 'decision'. The T cell-bias and B cell-bias transcriptional programs were frequently co-expressed in common lymphoid progenitor cells and were segregated in subsets biased toward T cell differentiation or B cell differentiation, after interleukin 7 (IL-7) signaling that controlled the number of progenitor cells engaging in T cell differentiation versus B cell differentiation.
[Mh] Termos MeSH primário: Linfócitos B/citologia
Linhagem da Célula
Fígado/citologia
Linfopoese
Linfócitos T/citologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/metabolismo
Biomarcadores
Diferenciação Celular/genética
Linhagem da Célula/genética
Análise por Conglomerados
Feto
Perfilação da Expressão Gênica
Regulação da Expressão Gênica no Desenvolvimento
Imunofenotipagem
Interleucina-7/metabolismo
Fígado/embriologia
Células Progenitoras Linfoides/citologia
Células Progenitoras Linfoides/metabolismo
Linfopoese/genética
Camundongos
Camundongos Transgênicos
Transdução de Sinais
Linfócitos T/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Interleukin-7)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3820


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[PMID]:28825697
[Au] Autor:Horton SJ; Giotopoulos G; Yun H; Vohra S; Sheppard O; Bashford-Rogers R; Rashid M; Clipson A; Chan WI; Sasca D; Yiangou L; Osaki H; Basheer F; Gallipoli P; Burrows N; Erdem A; Sybirna A; Foerster S; Zhao W; Sustic T; Petrunkina Harrison A; Laurenti E; Okosun J; Hodson D; Wright P; Smith KG; Maxwell P; Fitzgibbon J; Du MQ; Adams DJ; Huntly BJP
[Ad] Endereço:Wellcome Trust-MRC Cambridge Stem Cell Institute, Cambridge, UK.
[Ti] Título:Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors.
[So] Source:Nat Cell Biol;19(9):1093-1104, 2017 Sep.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Loss-of-function mutations of cyclic-AMP response element binding protein, binding protein (CREBBP) are prevalent in lymphoid malignancies. However, the tumour suppressor functions of CREBBP remain unclear. We demonstrate that loss of Crebbp in murine haematopoietic stem and progenitor cells (HSPCs) leads to increased development of B-cell lymphomas. This is preceded by accumulation of hyperproliferative lymphoid progenitors with a defective DNA damage response (DDR) due to a failure to acetylate p53. We identify a premalignant lymphoma stem cell population with decreased H3K27ac, which undergoes transcriptional and genetic evolution due to the altered DDR, resulting in lymphomagenesis. Importantly, when Crebbp is lost later in lymphopoiesis, cellular abnormalities are lost and tumour generation is attenuated. We also document that CREBBP mutations may occur in HSPCs from patients with CREBBP-mutated lymphoma. These data suggest that earlier loss of Crebbp is advantageous for lymphoid transformation and inform the cellular origins and subsequent evolution of lymphoid malignancies.
[Mh] Termos MeSH primário: Proteína de Ligação a CREB/deficiência
Proteína de Ligação a CREB/metabolismo
Transformação Celular Neoplásica/metabolismo
Células Progenitoras Linfoides/metabolismo
Linfoma/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Animais
Proteína de Ligação a CREB/genética
Proliferação Celular
Autorrenovação Celular
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/patologia
Células Cultivadas
Dano ao DNA
Epigênese Genética
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Histonas/metabolismo
Linfangiogênese
Células Progenitoras Linfoides/patologia
Linfoma/genética
Linfoma/patologia
Linfopoese
Metilação
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Mutação
Células-Tronco Neoplásicas/patologia
Fenótipo
Transdução de Sinais
Fatores de Tempo
Transcrição Genética
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histones); 0 (Tumor Suppressor Protein p53); EC 2.3.1.48 (CREB-Binding Protein); EC 2.3.1.48 (CREBBP protein, human); EC 2.3.1.48 (Crebbp protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3597


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[PMID]:28733485
[Au] Autor:Ghosh D; Brown SL; Stumhofer JS
[Ad] Endereço:Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
[Ti] Título:IL-17 Promotes Differentiation of Splenic LSK Lymphoid Progenitors into B Cells following Infection.
[So] Source:J Immunol;199(5):1783-1795, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lineage Sca-1 c-Kit (LSK ) cells are a lymphoid progenitor population that expands in the spleen and preferentially differentiates into mature B cells in response to infection in mice. Furthermore, LSK derived B cells can subsequently contribute to the ongoing immune response through the generation of parasite-specific Ab-secreting cells, as well as germinal center and memory B cells. However, the factors that promote their differentiation into B cells in the spleen postinfection are not defined. In this article, we show that LSK cells produce the cytokine IL-17 in response to infection. Using mice, IL-17R signaling in cells other than LSK cells was found to support their differentiation into B cells. Moreover, primary splenic stromal cells grown in the presence of IL-17 enhanced the production of CXCL12, a chemokine associated with B cell development in the bone marrow, by a population of IL-17RA-expressing podoplanin CD31 stromal cells, a profile associated with fibroblastic reticular cells. Subsequent blockade of CXCL12 in vitro reduced differentiation of LSK cells into B cells, supporting a direct role for this chemokine in this process. Immunofluorescence indicated that podoplanin stromal cells in the red pulp were the primary producers of CXCL12 after infection. Furthermore, podoplanin staining on stromal cells was more diffuse, and CXCL12 staining was dramatically reduced in mice postinfection. Together, these results identify a distinct pathway that supports lymphoid development in the spleen during acute infection.
[Mh] Termos MeSH primário: Células Produtoras de Anticorpos/fisiologia
Linfócitos B/fisiologia
Interleucina-17/metabolismo
Células Progenitoras Linfoides/fisiologia
Malária/imunologia
Plasmodium yoelii/imunologia
Baço/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antiprotozoários/metabolismo
Células Produtoras de Anticorpos/parasitologia
Linfócitos B/parasitologia
Diferenciação Celular
Células Cultivadas
Quimiocina CXCL12/metabolismo
Feminino
Seres Humanos
Memória Imunológica
Células Progenitoras Linfoides/parasitologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Proto-Oncogênicas pp60(c-src)/metabolismo
Receptores de Interleucina-17/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Protozoan); 0 (Chemokine CXCL12); 0 (Il17r protein, mouse); 0 (Interleukin-17); 0 (Receptors, Interleukin-17); EC 2.7.1.- (Matk protein, mouse); EC 2.7.10.2 (Proto-Oncogene Proteins pp60(c-src))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601972


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[PMID]:28514688
[Au] Autor:Miyazaki M; Miyazaki K; Chen K; Jin Y; Turner J; Moore AJ; Saito R; Yoshida K; Ogawa S; Rodewald HR; Lin YC; Kawamoto H; Murre C
[Ad] Endereço:Department of Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto 606-8507, Japan; Department of Molecular Biology, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: mmiyazaki@infront.kyoto-u.ac.jp.
[Ti] Título:The E-Id Protein Axis Specifies Adaptive Lymphoid Cell Identity and Suppresses Thymic Innate Lymphoid Cell Development.
[So] Source:Immunity;46(5):818-834.e4, 2017 May 16.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Innate and adaptive lymphoid development is orchestrated by the activities of E proteins and their antagonist Id proteins, but how these factors regulate early T cell progenitor (ETP) and innate lymphoid cell (ILC) development remains unclear. Using multiple genetic strategies, we demonstrated that E proteins E2A and HEB acted in synergy in the thymus to establish T cell identity and to suppress the aberrant development of ILCs, including ILC2s and lymphoid-tissue-inducer-like cells. E2A and HEB orchestrated T cell fate and suppressed the ILC transcription signature by activating the expression of genes associated with Notch receptors, T cell receptor (TCR) assembly, and TCR-mediated signaling. E2A and HEB acted in ETPs to establish and maintain a T-cell-lineage-specific enhancer repertoire, including regulatory elements associated with the Notch1, Rag1, and Rag2 loci. On the basis of these and previous observations, we propose that the E-Id protein axis specifies innate and adaptive lymphoid cell fate.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Imunidade Inata
Imunomodulação
Subpopulações de Linfócitos/imunologia
Timócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Diferenciação Celular/imunologia
Análise por Conglomerados
Expressão Gênica
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Redes Reguladoras de Genes
Imunofenotipagem
Proteína 2 Inibidora de Diferenciação/genética
Proteína 2 Inibidora de Diferenciação/metabolismo
Ativação Linfocitária/genética
Ativação Linfocitária/imunologia
Subpopulações de Linfócitos/citologia
Subpopulações de Linfócitos/metabolismo
Células Progenitoras Linfoides/metabolismo
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Fenótipo
Especificidade do Receptor de Antígeno de Linfócitos T/imunologia
Timócitos/citologia
Timócitos/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Inhibitor of Differentiation Protein 2); 0 (Tcf3 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE


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[PMID]:28390857
[Au] Autor:Lebert-Ghali CÉ; Thompson A; Melichar HJ; Bijl JJ
[Ad] Endereço:Maisonneuve-Rosemont Hospital Research Center, Montréal, QC, Canada; Department of Microbiology, Infectious Disease and Immunology, Université de Montréal, Montréal, QC, Canada.
[Ti] Título:Targeted deletion of the Hoxa cluster affects B lymphopoiesis through depletion of early lymphoid progenitors.
[So] Source:Exp Hematol;50:84-89.e3, 2017 Jun.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:It is well established that Hoxa genes play a critical role in the proliferative capacity of adult hematopoietic stem and progenitor cells, but the importance of Hoxa genes in later stages of hematopoietic differentiation is less clear. Previously, we observed that B-cell numbers were reduced in adult mice in which Hoxa deletion was induced. In the current study, we investigated the requirement of Hoxa genes at different stages of B-cell development. Using an MxCre-inducible conditional knock-out mouse model, we showed that immature B-cell fractions and early lymphoid progenitors were markedly reduced in the absence of Hoxa, whereas mature B-cell populations were found at levels comparable to controls. Deletion of Hoxa genes in B-cell lineage-committed cells, however, did not affect B-cell development despite sustained Hoxa gene expression in immature CD19 B-cell subsets. Together, these results suggest that the effect of Hoxa on B-cell development originates in early lymphoid progenitor cells.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Proteínas de Homeodomínio/genética
Células Progenitoras Linfoides/metabolismo
Linfopoese/genética
Família Multigênica
Deleção de Sequência
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Diferenciação Celular/genética
Regulação da Expressão Gênica no Desenvolvimento
Células Progenitoras Linfoides/citologia
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 157907-48-7 (HoxA protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170410
[St] Status:MEDLINE


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[PMID]:28347744
[Au] Autor:Seemann F; Peterson DR; Chiang MWL; Au DWT
[Ad] Endereço:State Key Laboratory in Marine Pollution, Department of Biology and Chemistry, City University of Hong Kong, Hong Kong Special Administrative Region.
[Ti] Título:The development of cellular immune defence in marine medaka Oryzias melastigma.
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;199:81-89, 2017 Sep.
[Is] ISSN:1532-0456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Environmentally induced alterations of the immune system during sensitive developmental stages may manifest as abnormalities in immune organ configuration and/or immune cell differentiation. These not only render the early life stages more vulnerable to pathogens, but may also affect the adult immune competence. Knowledge of these sensitive periods in fish would provide an important prognostic/diagnostic tool for aquatic risk assessment of immunotoxicants. The marine medaka Oryzias melastigma is an emerging seawater fish model for immunotoxicology. Here, the presence and onset of four potentially sensitive periods during the development of innate and adaptive cellular immune defence were revealed in O. melastigma: 1.) initiation of phagocyte differentiation, 2.) migration and expansion of lymphoid progenitor cells, 3.) colonization of immune organs through lymphocyte progenitors and 4.) establishment of immune competence in the thymus. By using an established bacterial resistance assay for O. melastigma, larval immune competence (from newly hatched 1dph to 14dph) was found concomitantly increased with advanced thymus development and the presence of mature T-lymphocytes. A comparison between the marine O. melastigma and the freshwater counterpart Oryzias latipes disclosed a disparity in the T-lymphocyte maturation pattern, resulting in differences in the length of T-lymphocyte maturation. The results shed light on a potential difference between seawater and freshwater medaka in their sensitivity to environmental immunotoxicants. Further, medaka immune system development was compared and contrasted to economically important fish. The present study has provided a strong scientific basis for advanced investigation of critical windows for immune system development in fish.
[Mh] Termos MeSH primário: Embrião não Mamífero/imunologia
Imunidade Celular
Imunidade Inata
Imunocompetência
Larva/imunologia
Morfogênese
Oryzias/imunologia
[Mh] Termos MeSH secundário: Animais
Aquicultura
Carga Bacteriana
Diferenciação Celular
Edwardsiella tarda/crescimento & desenvolvimento
Edwardsiella tarda/imunologia
Edwardsiella tarda/isolamento & purificação
Embrião não Mamífero/citologia
Embrião não Mamífero/microbiologia
Desenvolvimento Embrionário
Regulação da Expressão Gênica no Desenvolvimento
Rim Cefálico/citologia
Rim Cefálico/crescimento & desenvolvimento
Rim Cefálico/imunologia
Rim Cefálico/microbiologia
Hibridização In Situ/veterinária
Larva/citologia
Larva/crescimento & desenvolvimento
Larva/microbiologia
Células Progenitoras Linfoides/citologia
Células Progenitoras Linfoides/imunologia
Células Progenitoras Linfoides/microbiologia
Oryzias/embriologia
Oryzias/crescimento & desenvolvimento
Oryzias/microbiologia
Fagócitos/citologia
Fagócitos/imunologia
Fagócitos/microbiologia
Especificidade da Espécie
Baço/citologia
Baço/crescimento & desenvolvimento
Baço/imunologia
Baço/microbiologia
Análise de Sobrevida
Linfócitos T/citologia
Linfócitos T/imunologia
Linfócitos T/microbiologia
Timo/citologia
Timo/crescimento & desenvolvimento
Timo/imunologia
Timo/microbiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE



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