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[PMID]:29430664
[Au] Autor:Budzynska PM; Kyläniemi MK; Lassila O; Nera KP; Alinikula J
[Ad] Endereço:Department of Medical Microbiology and Immunology, Institute of Biomedicine, University of Turku, Turku, Finland.
[Ti] Título:BLIMP-1 is insufficient to induce antibody secretion in the absence of IRF4 in DT40 cells.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Differentiation of B cells into antibody-secreting cells (ASCs), plasmablasts and plasma cells is regulated by a network of transcription factors. Within this network, factors including PAX5 and BCL6 prevent ASC differentiation and maintain the B cell phenotype. In contrast, BLIMP-1 and high IRF4 expression promote plasma cell differentiation. BLIMP-1 is thought to induce immunoglobulin secretion, whereas IRF4 is needed for the survival of ASCs. The role of IRF4 in the regulation of antibody secretion has remained controversial. To study the role of IRF4 in the regulation of antibody secretion, we have created a double knockout (DKO) DT40 B cell line deficient in both IRF4 and BCL6. Although BCL6-deficient DT40 B cell line had upregulated BLIMP-1 expression and secreted antibodies, the DKO cell line did not. Even enforced BLIMP-1 expression in DKO cells or IRF4-deficient cells could not induce IgM secretion while in WT DT40 cells, it could. However, enforced IRF4 expression in DKO cells induced strong IgM secretion. Our findings support a model where IRF4 expression in addition to BLIMP-1 expression is required to induce robust antibody secretion.
[Mh] Termos MeSH primário: Anticorpos/imunologia
Formação de Anticorpos/genética
Proteínas Aviárias/genética
Linfócitos B/imunologia
Fatores Reguladores de Interferon/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
[Mh] Termos MeSH secundário: Animais
Linfócitos B/citologia
Diferenciação Celular/imunologia
Linhagem Celular
Proliferação Celular
Galinhas
Técnicas de Inativação de Genes
Imunoglobulina M/biossíntese
Imunoglobulina M/imunologia
Fator de Transcrição PAX5/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/imunologia
Proteínas Proto-Oncogênicas c-bcl-6/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Avian Proteins); 0 (IRF4 protein, Gallus gallus); 0 (Immunoglobulin M); 0 (Interferon Regulatory Factors); 0 (PAX5 Transcription Factor); 0 (Proto-Oncogene Proteins c-bcl-6); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12646


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[PMID]:29325247
[Au] Autor:Zhang XY; Ma ZP; Cui WL; Pang XL; Chen R; Wang L; Zhang W; Li XX
[Ad] Endereço:Department of Pathology, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China.
[Ti] Título:[Impact of PRDM1 gene inactivation on C-MYC regulation in diffuse large B-cell lymphoma].
[So] Source:Zhonghua Bing Li Xue Za Zhi;47(1):25-31, 2018 Jan 08.
[Is] ISSN:0529-5807
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the role of PRDM1 gene inactivaion in the regulation of C-MYC in diffuse large B-cell lymphoma (DLBCL), and to explore the correlation of its immunophenotype and prognosis. 100 cases paraffin-embedded DLBCL tissues were collected from January 2009 to December 2015 at the First Affiliated Hospital of Xinjiang Medical University along with 20 cases of reactive proliferative lymph nodes as control. Immunohistochemical methods were used to detect the expression of CD20, CD10, MUM1, Ki-67, bcl-6, PRDM1/Blimp1, C-MYC and PAX5 protein. The tumors were classified into two subtypes according to Hans classification.The expression of PRDM1 and C-MYC gene in tumor group and control group was detected by reverse transcription PCR (RT-PCR) and the relationship between PRDM1 and C-MYC gene was analyzed.OCI-LY1 (GCB subtype) and OCI-LY3 (non-GCB subtype) cell lines were transfected with small interfering RNA by cationic liposome reagent transfection, and the expression of C-MYC in the transfected cell lines was detected by RT-PCR and Western blot. The Kaplan-Meier method was used to analyze the prognostic significance of PRDM1/Blimp1 and C-MYC at protein and mRNA levels. There were 27 cases of GCB subtype and 73 cases of non-GCB subtype according to Hans classification. The positive expression of Blimp1 in DLBCL group and proliferative lymph nodes in control group was seen in 26(26.0%) and 20 cases(100%), respectively. There were 58 cases with high expression of PRDM1 at mRNA level, including 22 cases of GCB subtype and 36 cases non-GCB subtype, and the difference was statistically significant ( =0.004). There were differences in PRDM1 gene expression between the two immunological subtypes, serum lactate dehydrogenase (serum LDH) level, presence of B symptoms, tumor primary sites and other clinical pathological parameters, while C-MYC expression was different in gender, IPI score, and serum LDH levels. Upon PRDM1/Blimp1 gene silencing in the two cell lines, C-MYC protein and gene expression were up-regulated in the transfection group, compared with the blank control group and negative control group by reverse transcription PCR and Western blot analyses. Moreover, PRDM1 expression was significantly associated with C-MYC(χ(2)=7.648, =0.006) at mRNA level. The up-regulation of C-MYC gene expression induced by PRDM1 inactivation in DLBCL may play an important role for the development of DLBCL.PRDM1 protein and mRNA are associated with immunophenotyping and PRDM1 mRNA is a marker of poor prognosis.
[Mh] Termos MeSH primário: Inativação Gênica
Genes myc
Linfoma Difuso de Grandes Células B/genética
Fator 1 de Ligação ao Domínio I Regulador Positivo/genética
[Mh] Termos MeSH secundário: Antígenos CD20/metabolismo
Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Imunofenotipagem
Linfonodos/patologia
Linfoma Difuso de Grandes Células B/patologia
Fator de Transcrição PAX5/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
RNA Mensageiro/metabolismo
Proteínas Repressoras/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD20); 0 (PAX5 Transcription Factor); 0 (PAX5 protein, human); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Proto-Oncogene Proteins c-myc); 0 (RNA, Messenger); 0 (Repressor Proteins); 138415-26-6 (PRDM1 protein, human); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-5807.2018.01.006


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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]:28930664
[Au] Autor:Goudot C; Coillard A; Villani AC; Gueguen P; Cros A; Sarkizova S; Tang-Huau TL; Bohec M; Baulande S; Hacohen N; Amigorena S; Segura E
[Ad] Endereço:Institut Curie, PSL Research University, INSERM, U932, 26 rue d'Ulm, 75005 Paris, France.
[Ti] Título:Aryl Hydrocarbon Receptor Controls Monocyte Differentiation into Dendritic Cells versus Macrophages.
[So] Source:Immunity;47(3):582-596.e6, 2017 Sep 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:After entering tissues, monocytes differentiate into cells that share functional features with either macrophages or dendritic cells (DCs). How monocyte fate is directed toward monocyte-derived macrophages (mo-Macs) or monocyte-derived DCs (mo-DCs) and which transcription factors control these differentiation pathways remains unknown. Using an in vitro culture model yielding human mo-DCs and mo-Macs closely resembling those found in vivo in ascites, we show that IRF4 and MAFB were critical regulators of monocyte differentiation into mo-DCs and mo-Macs, respectively. Activation of the aryl hydrocarbon receptor (AHR) promoted mo-DC differentiation through the induction of BLIMP-1, while impairing differentiation into mo-Macs. AhR deficiency also impaired the in vivo differentiation of mouse mo-DCs. Finally, AHR activation correlated with mo-DC infiltration in leprosy lesions. These results establish that mo-DCs and mo-Macs are controlled by distinct transcription factors and show that AHR acts as a molecular switch for monocyte fate specification in response to micro-environmental factors.
[Mh] Termos MeSH primário: Células Dendríticas/metabolismo
Macrófagos/metabolismo
Monócitos/metabolismo
Receptores de Hidrocarboneto Arílico/metabolismo
[Mh] Termos MeSH secundário: Animais
Ascite
Células Cultivadas
Análise por Conglomerados
Citocinas/metabolismo
Citocinas/farmacologia
Células Dendríticas/citologia
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Feminino
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Seres Humanos
Fatores Reguladores de Interferon/metabolismo
Hanseníase/imunologia
Hanseníase/metabolismo
Hanseníase/microbiologia
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Fator de Transcrição MafB/metabolismo
Masculino
Camundongos
Camundongos Knockout
Monócitos/citologia
Monócitos/efeitos dos fármacos
Monócitos/imunologia
Neoplasias/genética
Neoplasias/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo
Receptores de Hidrocarboneto Arílico/genética
Proteínas Repressoras/metabolismo
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interferon Regulatory Factors); 0 (MafB Transcription Factor); 0 (Receptors, Aryl Hydrocarbon); 0 (Repressor Proteins); 0 (interferon regulatory factor-4); 138415-26-6 (PRDM1 protein, human); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[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:170921
[St] Status:MEDLINE


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[PMID]:28928204
[Au] Autor:Miyauchi H; Ohta H; Nagaoka S; Nakaki F; Sasaki K; Hayashi K; Yabuta Y; Nakamura T; Yamamoto T; Saitou M
[Ad] Endereço:Department of Anatomy and Cell Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
[Ti] Título:Bone morphogenetic protein and retinoic acid synergistically specify female germ-cell fate in mice.
[So] Source:EMBO J;36(21):3100-3119, 2017 Nov 02.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mechanism for sex determination in mammalian germ cells remains unclear. Here, we reconstitute the female sex determination in mouse germ cells under a defined condition without the use of gonadal somatic cells. We show that retinoic acid (RA) and its key effector, STRA8, are not sufficient to induce the female germ-cell fate. In contrast, bone morphogenetic protein (BMP) and RA synergistically induce primordial germ cells (PGCs)/PGC-like cells (PGCLCs) derived from embryonic stem cells (ESCs) into fetal primary oocytes. The induction is characterized by entry into the meiotic prophase, occurs synchronously and recapitulates cytological and transcriptome progression faithfully. Importantly, the female germ-cell induction necessitates a proper cellular competence-most typically, DNA demethylation of relevant genes-which is observed in appropriately propagated PGCs/PGCLCs, but not in PGCs/PGCLCs immediately after induction. This provides an explanation for the differential function of BMP signaling between PGC specification and female germ-cell induction. Our findings represent a framework for a comprehensive delineation of the sex-determination pathway in mammalian germ cells, including humans.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Morfogenéticas Ósseas/farmacologia
Regulação da Expressão Gênica no Desenvolvimento
Células-Tronco Embrionárias Murinas/efeitos dos fármacos
Oócitos/efeitos dos fármacos
Tretinoína/farmacologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Animais
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Proteínas Morfogenéticas Ósseas/genética
Proteínas Morfogenéticas Ósseas/metabolismo
Diferenciação Celular
Feminino
Feto
Perfilação da Expressão Gênica
Genes Reporter
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos
Camundongos Endogâmicos ICR
Células-Tronco Embrionárias Murinas/citologia
Células-Tronco Embrionárias Murinas/metabolismo
Oócitos/citologia
Oócitos/crescimento & desenvolvimento
Oócitos/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo
Prófase
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Processos de Determinação Sexual
Transdução de Sinais
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Bacterial Proteins); 0 (Bone Morphogenetic Proteins); 0 (Luminescent Proteins); 0 (Prdm1 protein, mouse); 0 (Protein Isoforms); 0 (Stra8 protein, mouse); 0 (Transcription Factors); 0 (yellow fluorescent protein, Bacteria); 5688UTC01R (Tretinoin); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201796875


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[PMID]:28892471
[Au] Autor:Botta D; Fuller MJ; Marquez-Lago TT; Bachus H; Bradley JE; Weinmann AS; Zajac AJ; Randall TD; Lund FE; León B; Ballesteros-Tato A
[Ad] Endereço:Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
[Ti] Título:Dynamic regulation of T follicular regulatory cell responses by interleukin 2 during influenza infection.
[So] Source:Nat Immunol;18(11):1249-1260, 2017 Nov.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin 2 (IL-2) promotes Foxp3 regulatory T (T ) cell responses, but inhibits T follicular helper (T ) cell development. However, it is not clear how IL-2 affects T follicular regulatory (T ) cells, a cell type with properties of both T and T cells. Using an influenza infection model, we found that high IL-2 concentrations at the peak of the infection prevented T cell development by a Blimp-1-dependent mechanism. However, once the immune response resolved, some T cells downregulated CD25, upregulated Bcl-6 and differentiated into T cells, which then migrated into the B cell follicles to prevent the expansion of self-reactive B cell clones. Thus, unlike its effects on conventional T cells, IL-2 inhibits T cell responses.
[Mh] Termos MeSH primário: Interleucina-2/farmacologia
Infecções por Orthomyxoviridae/imunologia
Orthomyxoviridae/imunologia
Linfócitos T Auxiliares-Indutores/efeitos dos fármacos
Linfócitos T Reguladores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Movimento Celular/genética
Movimento Celular/imunologia
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Perfilação da Expressão Gênica/métodos
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Interações Hospedeiro-Patógeno/imunologia
Interleucina-2/administração & dosagem
Interleucina-2/metabolismo
Subunidade alfa de Receptor de Interleucina-2/genética
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Orthomyxoviridae/fisiologia
Infecções por Orthomyxoviridae/metabolismo
Infecções por Orthomyxoviridae/virologia
Fator 1 de Ligação ao Domínio I Regulador Positivo
Proteínas Proto-Oncogênicas c-bcl-6/genética
Proteínas Proto-Oncogênicas c-bcl-6/metabolismo
Linfócitos T Auxiliares-Indutores/imunologia
Linfócitos T Auxiliares-Indutores/metabolismo
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/imunologia
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Prdm1 protein, mouse); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Transcription Factors); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3837


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[PMID]:28835458
[Au] Autor:Corpuz TM; Vazquez-Lombardi R; Luong JK; Warren J; Stolp J; Christ D; King C; Brink R; Sprent J; Webster KE
[Ad] Endereço:Immunology Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales 2010, Australia; and.
[Ti] Título:IL-2 Shapes the Survival and Plasticity of IL-17-Producing γδ T Cells.
[So] Source:J Immunol;199(7):2366-2376, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-17-producing γδ T (γδT-17) cells have proved to be an important early source of IL-17 in many inflammatory settings and are emerging as an important participant in protumor immune responses. Considering that their peripheral activation depends largely on innate signals rather than TCR ligation, it is important to understand what mechanisms exist to curb unwanted activation. Expression of the high-affinity IL-2R on γδT-17 cells prompted us to investigate a role for this cytokine. We found γδT-17 cells to be enriched, not depleted, in IL-2-deficient mice. The absence of IL-2 also resulted in higher IL-17 production and the emergence of IL-17 IFN-γ double producers. Furthermore, the addition of IL-2 to in vitro cultures of sorted γδT-17 cells was able to moderate IL-17 and affect differentiation into polyfunctional cytokine-producing cells. Interestingly, the Vγ6 subset was more susceptible to the effects of IL-2 than Vγ4 γδT-17 cells. We also found that unlike other γδ T cells, γδT-17 cells do not produce IL-2, but express Blimp-1, a known transcriptional repressor of IL-2. Although IL-2 was able to induce robust proliferation of γδT-17 cells, it did not sustain viability, negatively impacting their survival via downregulation of the IL-7R. Taken together, these data indicate that IL-2 can augment the γδT-17 response in favor of short-lived effectors with limited plasticity, particularly in the presence of IL-1ß and IL-23. In this way, IL-2 may act to curtail the innate-like response of γδT-17 cells upon arrival of IL-2-producing adaptive immune cells at the site of inflammation.
[Mh] Termos MeSH primário: Interleucina-17/biossíntese
Interleucina-2/imunologia
Interleucina-2/metabolismo
Receptores de Antígenos de Linfócitos T gama-delta/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Citocinas/biossíntese
Citometria de Fluxo
Inflamação
Interferon gama/biossíntese
Interferon gama/imunologia
Interleucina-17/imunologia
Interleucina-2/deficiência
Interleucina-2/genética
Interleucina-23/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Fator 1 de Ligação ao Domínio I Regulador Positivo
Receptores de Interleucina-7/genética
Transdução de Sinais
Linfócitos T/efeitos dos fármacos
Linfócitos T/fisiologia
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-17); 0 (Interleukin-2); 0 (Interleukin-23); 0 (Prdm1 protein, mouse); 0 (Receptors, Antigen, T-Cell, gamma-delta); 0 (Receptors, Interleukin-7); 0 (Transcription Factors); 82115-62-6 (Interferon-gamma); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700335


  8 / 615 MEDLINE  
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[PMID]:28829770
[Au] Autor:Mills TS; Eliseeva T; Bersie SM; Randazzo G; Nahreini J; Park KU; Brzezinski JA
[Ad] Endereço:Department of Ophthalmology, University of Colorado Denver, Aurora, CO, United States of America.
[Ti] Título:Combinatorial regulation of a Blimp1 (Prdm1) enhancer in the mouse retina.
[So] Source:PLoS One;12(8):e0176905, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mouse retina comprises seven major cell types that exist in differing proportions. They are generated from multipotent progenitors in a stochastic manner, such that the relative frequency of any given type generated changes over time. The mechanisms determining the proportions of each cell type are only partially understood. Photoreceptors and bipolar interneurons are derived from cells that express Otx2. Within this population, Blimp1 (Prdm1) helps set the balance between photoreceptors and bipolar cells by suppressing bipolar identity in most of the cells. How only a subset of these Otx2+ cells decides to upregulate Blimp1 and adopt photoreceptor fate is unknown. To understand this, we investigated how Blimp1 transcription is regulated. We identified several potential Blimp1 retinal enhancer elements using DNase hypersensitivity sequencing. Only one of the elements recapitulated Blimp1 spatial and temporal expression in cultured explant assays and within the retinas of transgenic mice. Mutagenesis of this retinal Blimp1 enhancer element revealed four discrete sequences that were each required for its activity. These included highly conserved Otx2 and ROR (retinoic acid receptor related orphan receptor) binding sites. The other required sequences do not appear to be controlled by Otx2 or ROR factors, increasing the complexity of the Blimp1 gene regulatory network. Our results show that the intersection of three or more transcription factors is required to correctly regulate the spatial and temporal features of Blimp1 enhancer expression. This explains how Blimp1 expression can diverge from Otx2 and set the balance between photoreceptor and bipolar fates.
[Mh] Termos MeSH primário: Elementos Facilitadores Genéticos
Retina/metabolismo
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Endogâmicos C57BL
Fator 1 de Ligação ao Domínio I Regulador Positivo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prdm1 protein, mouse); 0 (Transcription Factors); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[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:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176905


  9 / 615 MEDLINE  
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[PMID]:28771465
[Au] Autor:Styles CT; Bazot Q; Parker GA; White RE; Paschos K; Allday MJ
[Ad] Endereço:Molecular Virology, Department of Medicine, Imperial College London, London, United Kingdom.
[Ti] Título:EBV epigenetically suppresses the B cell-to-plasma cell differentiation pathway while establishing long-term latency.
[So] Source:PLoS Biol;15(8):e2001992, 2017 Aug.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mature human B cells infected by Epstein-Barr virus (EBV) become activated, grow, and proliferate. If the cells are infected ex vivo, they are transformed into continuously proliferating lymphoblastoid cell lines (LCLs) that carry EBV DNA as extra-chromosomal episomes, express 9 latency-associated EBV proteins, and phenotypically resemble antigen-activated B-blasts. In vivo similar B-blasts can differentiate to become memory B cells (MBC), in which EBV persistence is established. Three related latency-associated viral proteins EBNA3A, EBNA3B, and EBNA3C are transcription factors that regulate a multitude of cellular genes. EBNA3B is not necessary to establish LCLs, but EBNA3A and EBNA3C are required to sustain proliferation, in part, by repressing the expression of tumour suppressor genes. Here we show, using EBV-recombinants in which both EBNA3A and EBNA3C can be conditionally inactivated or using virus completely lacking the EBNA3 gene locus, that-after a phase of rapid proliferation-infected primary B cells express elevated levels of factors associated with plasma cell (PC) differentiation. These include the cyclin-dependent kinase inhibitor (CDKI) p18INK4c, the master transcriptional regulator of PC differentiation B lymphocyte-induced maturation protein-1 (BLIMP-1), and the cell surface antigens CD38 and CD138/Syndecan-1. Chromatin immunoprecipitation sequencing (ChIP-seq) and chromatin immunoprecipitation quantitative PCR (ChIP-qPCR) indicate that in LCLs inhibition of CDKN2C (p18INK4c) and PRDM1 (BLIMP-1) transcription results from direct binding of EBNA3A and EBNA3C to regulatory elements at these loci, producing stable reprogramming. Consistent with the binding of EBNA3A and/or EBNA3C leading to irreversible epigenetic changes, cells become committed to a B-blast fate <12 days post-infection and are unable to de-repress p18INK4c or BLIMP-1-in either newly infected cells or conditional LCLs-by inactivating EBNA3A and EBNA3C. In vitro, about 20 days after infection with EBV lacking functional EBNA3A and EBNA3C, cells develop a PC-like phenotype. Together, these data suggest that EBNA3A and EBNA3C have evolved to prevent differentiation to PCs after infection by EBV, thus favouring long-term latency in MBC and asymptomatic persistence.
[Mh] Termos MeSH primário: Linfócitos B/virologia
Infecções por Vírus Epstein-Barr/imunologia
Herpesvirus Humano 4/fisiologia
Proteínas Virais/fisiologia
Latência Viral
[Mh] Termos MeSH secundário: Linfócitos B/fisiologia
Biomarcadores/metabolismo
Diferenciação Celular
Linhagem Celular Tumoral
Inibidor de Quinase Dependente de Ciclina p18/metabolismo
Código das Histonas
Seres Humanos
Imunoglobulinas/metabolismo
Plasmócitos/metabolismo
Fator 1 de Ligação ao Domínio I Regulador Positivo
Proteínas Repressoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cyclin-Dependent Kinase Inhibitor p18); 0 (Immunoglobulins); 0 (Repressor Proteins); 0 (Viral Proteins); 138415-26-6 (PRDM1 protein, human); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001992


  10 / 615 MEDLINE  
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[PMID]:28768724
[Au] Autor:McKay JT; Haro MA; Daly CA; Yammani RD; Pang B; Swords WE; Haas KM
[Ad] Endereço:Department of Microbiology and Immunology, Wake Forest School of Medicine, Winston-Salem, NC 27157.
[Ti] Título:PD-L2 Regulates B-1 Cell Antibody Production against Phosphorylcholine through an IL-5-Dependent Mechanism.
[So] Source:J Immunol;199(6):2020-2029, 2017 Sep 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:B-1 cells produce natural Abs which provide an integral first line of defense against pathogens while also performing important homeostatic housekeeping functions. In this study, we demonstrate that programmed cell death 1 ligand 2 (PD-L2) regulates the production of natural Abs against phosphorylcholine (PC). Naive PD-L2-deficient (PD-L2 ) mice produced significantly more PC-reactive IgM and IgA. This afforded PD-L2 mice with selectively enhanced protection against PC-expressing nontypeable , but not PC-negative nontypeable , relative to wild-type mice. PD-L2 mice had significantly increased PC-specific CD138 splenic plasmablasts bearing a B-1a phenotype, and produced PC-reactive Abs largely of the T15 Id. Importantly, PC-reactive B-1 cells expressed PD-L2 and irradiated chimeras demonstrated that B cell-intrinsic PD-L2 expression regulated PC-specific Ab production. In addition to increased PC-specific IgM, naive PD-L2 mice and irradiated chimeras reconstituted with PD-L2 B cells had significantly higher levels of IL-5, a potent stimulator of B-1 cell Ab production. PD-L2 mAb blockade of wild-type B-1 cells in culture significantly increased CD138 and Blimp1 expression and PC-specific IgM, but did not affect proliferation. PD-L2 mAb blockade significantly increased IL-5 T cells in culture. Both IL-5 neutralization and STAT5 inhibition blunted the effects of PD-L2 mAb blockade on B-1 cells. Thus, B-1 cell-intrinsic PD-L2 expression inhibits IL-5 production by T cells and thereby limits natural Ab production by B-1 cells. These findings have broad implications for the development of therapeutic strategies aimed at altering natural Ab levels critical for protection against infectious disease, autoimmunity, allergy, cancer, and atherosclerosis.
[Mh] Termos MeSH primário: Formação de Anticorpos
Linfócitos B/imunologia
Imunoglobulina M/metabolismo
Fosforilcolina/imunologia
Proteína 2 Ligante de Morte Celular Programada 1/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Bloqueadores/farmacologia
Diferenciação Celular
Proliferação Celular
Células Cultivadas
Homeostase
Imunidade Inata
Interleucina-5/metabolismo
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fator 1 de Ligação ao Domínio I Regulador Positivo
Proteína 2 Ligante de Morte Celular Programada 1/imunologia
Sindecana-1/genética
Sindecana-1/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Blocking); 0 (Immunoglobulin M); 0 (Interleukin-5); 0 (Pdcd1lg2 protein, mouse); 0 (Prdm1 protein, mouse); 0 (Programmed Cell Death 1 Ligand 2 Protein); 0 (Syndecan-1); 0 (Transcription Factors); 107-73-3 (Phosphorylcholine); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700555



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