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[PMID]: 29362889 [Au] Autor: Gaudio F; Tamma R; Ingravallo G; Perrone T; Laddaga FE; De Candia M; Maiorano E; Ribatti D; Specchia G [Ad] Endereço: Department of Emergency and Organ Transplantation (D.E.T.O.), Hematology Section, University of Bari, Bari, Italy. fragaudio@alice.it. [Ti] Título: Computer-driven quantitative image analysis in the assessment of tumor cell and T cell features in diffuse large B cell lymphomas. [So] Source: Ann Hematol;97(4):663-668, 2018 Apr. [Is] ISSN: 1432-0584 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: Diffuse large B cell lymphoma (DLBCL) is recognized as the most common non-Hodgkin lymphoma subtype. Advanced high-resolution digital scans of pathology slides have enabled the development of computer-based image analysis algorithms that may assist pathologists in quantifying immunohistochemical stains. In this retrospective study, we reviewed data from 29 patients affected by DLBCL. In order to evaluate the number of tumor cells and microenvironment T cells, we performed an analysis of CD20, Ki67, and CD3 counts, assessed with the Positive Pixel Count algorithm embedded in the Aperio ImageScope software. A lower tumor cell count was observed in patients with a non-germinal center immunophenotype, high LDH, splenomegaly and an IPI ≥ 3. A lower number of CD3 was observed in patients with bulky disease, an IPI ≥ 3 and disease stage 3-4. Overall, these data confirm that quantitative analysis of the tumor cells and of the tumor microenvironment by means of computer-driven quantitative image analysis may add new information in DLBCL diagnosis. [Mh] Termos MeSH primário: Linfócitos B/patologia Interpretação de Imagem Assistida por Computador Linfonodos/diagnóstico por imagem Linfoma Difuso de Grandes Células B/diagnóstico por imagem Linfócitos T/patologia [Mh] Termos MeSH secundário: Adulto Idoso Idoso de 80 Anos ou mais Algoritmos Antígenos CD20/metabolismo Linfócitos B/imunologia Linfócitos B/metabolismo Complexo CD3/metabolismo Feminino Centro Germinativo/imunologia Centro Germinativo/metabolismo Centro Germinativo/patologia Seres Humanos Imuno-Histoquímica Antígeno Ki-67/metabolismo Linfonodos/imunologia Linfonodos/metabolismo Linfonodos/patologia Linfoma Difuso de Grandes Células B/imunologia Linfoma Difuso de Grandes Células B/metabolismo Linfoma Difuso de Grandes Células B/patologia Masculino Meia-Idade Estadiamento de Neoplasias Prognóstico Estudos Retrospectivos Linfócitos T/imunologia Linfócitos T/metabolismo Microambiente Tumoral [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antigens, CD20); 0 (CD3 Complex); 0 (Ki-67 Antigen) [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: 180125 [St] Status: MEDLINE [do] DOI: 10.1007/s00277-017-3212-6

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[PMID]: 28922789 [Au] Autor: Mlecnik B; Van den Eynde M; Bindea G; Church SE; Vasaturo A; Fredriksen T; Lafontaine L; Haicheur N; Marliot F; Debetancourt D; Pairet G; Jouret-Mourin A; Gigot JF; Hubert C; Danse E; Dragean C; Carrasco J; Humblet Y; Valge-Archer V; Berger A; Pagès F; Machiels JP; Galon J [Ad] Endereço: Laboratory of Integrative Cancer Immunology, INSERM, UMRS1138, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, UMRS1138, Paris, France; Sorbonne Universités, UPMC Univ Paris 06, UMRS1138, Centre de Recherche des Cordeliers, Paris, France; Inovarion, Paris, France; Department of Medic [Ti] Título: Comprehensive Intrametastatic Immune Quantification and Major Impact of Immunoscore on Survival. [So] Source: J Natl Cancer Inst;110(1), 2018 Jan 01. [Is] ISSN: 1460-2105 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Background: This study assesses how the metastatic immune landscape is impacting the response to treatment and the outcome of colorectal cancer (CRC) patients. Methods: Complete curative resection of metastases (n = 441) was performed for two patient cohorts (n = 153). Immune densities were quantified in the center and invasive margin of all metastases. Immunoscore and T and B cell (TB) score were analyzed in relation to radiological and pathological responses and patient's disease-free (DFS) and overall survival (OS) using multivariable Cox proportional hazards models. All statistical tests were two-sided. Results: The spatial distribution of immune cells within metastases was nonuniform. Patients, as well as metastases of the same patient, had variable immune infiltrates and response to therapy. A beneficial response was statistically significantly associated with increased immune densities. Among all metastases, Immunoscore (I) and TB score evaluated in the least immune-infiltrated metastases were the strongest predictors for DFS and OS (five-year follow-up, Immunoscore: I 3-4: DFS rate = 27.9%, 95% CI = 15.2 to 51.3; vs I 0-1-2: DFS rate = 12.3%, 95% CI = 4.9 to 30.6; HR = 0.45, 95% CI = 0.28 to 0.70, P = .02; I 3-4: OS rate = 64.6%, 95% CI = 46.6 to 89.6; vs I 0-1-2: OS rate = 32.5%, 95% CI = 17.2 to 61.4; HR = 0.32, 95% CI = 0.15 to 0.66, P = .001, C-index = 65.9%; five-year follow-up, TB score: TB 3-4: DFS rate = 25.7%, 95% CI = 14.2 to 46.6; vs TB 0-1-2: DFS rate = 5.0%, 95% CI = 0.8 to 32.4; HR = 0.36, 95% CI = 0.22 to 0.57, P < .001; TB 3-4: OS rate = 63.7%, 95% CI = 46.4 to 87.5; vs TB 0-1-2: OS rate: 21.4%, 95% CI = 9.2 to 49.8; HR = 0.25, 95% CI = 0.12 to 0.51, P < .001, C-index = 67.8%). High TB score and Immunoscore patients had a median survival of 70.5 months, while low patients survived only 25.1 to 38.3 months. Nonresponding patients with high-immune infiltrates had prolonged DFS (HR = 0.28, 95% CI = 0.15 to 0.52, P = .001) and OS (HR = 0.25, 95% CI = 0.1 to 0.62, P = .001). The immune parameters remained the only statistically significant prognostic factor associated with DFS and OS in multivariable analysis (P < .001), while response to treatment was not. Conclusions: Response to treatment and prolonged survival of metastatic CRC patients were statistically significantly associated with high-immune densities quantified into the least immune-infiltrated metastasis. [Mh] Termos MeSH primário: Linfócitos B Neoplasias Colorretais/imunologia Neoplasias Hepáticas/imunologia Neoplasias Pulmonares/imunologia Linfócitos do Interstício Tumoral Linfócitos T [Mh] Termos MeSH secundário: Idoso Antígenos CD20/análise Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico Linfócitos B/química Complexo CD3/análise Linfócitos T CD8-Positivos Quimioterapia Adjuvante Neoplasias Colorretais/patologia Neoplasias Colorretais/terapia Intervalo Livre de Doença Seguimentos Fatores de Transcrição Forkhead/análise Hepatectomia Seres Humanos Antígenos Comuns de Leucócito/análise Neoplasias Hepáticas/secundário Neoplasias Hepáticas/terapia Neoplasias Pulmonares/secundário Neoplasias Pulmonares/terapia Contagem de Linfócitos Metastasectomia Meia-Idade Metástase Neoplásica Pneumonectomia Período Pré-Operatório Critérios de Avaliação de Resposta em Tumores Sólidos Taxa de Sobrevida Linfócitos T/química Microambiente Tumoral/imunologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antigens, CD20); 0 (CD3 Complex); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); EC 3.1.3.48 (Leukocyte Common Antigens) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 180308 [Lr] Data última revisão: 180308 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170920 [St] Status: MEDLINE [do] DOI: 10.1093/jnci/djx123

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[PMID]: 28465009 [Au] Autor: Dong G; Kalifa R; Nath PR; Babichev Y; Gelkop S; Isakov N [Ad] Endereço: The Shraga Segal Department of Microbiology, Immunology and Genetics, Faculty of Health Sciences and the Cancer Research Center, Ben Gurion University of the Negev, P.O.B. 653, Beer Sheva 84105, Israel. Electronic address: gdong@upenn.edu. [Ti] Título: Crk adaptor proteins regulate CD3ζ chain phosphorylation and TCR/CD3 down-modulation in activated T cells. [So] Source: Cell Signal;36:117-126, 2017 Aug. [Is] ISSN: 1873-3913 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: T cell receptor (TCR) recognition of a peptide antigen in the context of MHC molecules initiates positive and negative cascades that regulate T cell activation, proliferation and differentiation, and culminate in the acquisition of effector T cell functions. These processes are a prerequisite for the induction of specific T cell-mediated adaptive immune responses. A key event in the activation of TCR-coupled signaling pathways is the phosphorylation of tyrosine residues within the cytoplasmic tails of the CD3 subunits, predominantly CD3ζ. These transiently formed phosphotyrosyl epitopes serve as docking sites for SH2-domain containing effector molecules, predominantly the ZAP70 protein tyrosine kinase, which is critical for signal propagation. We found that CrkI and CrkII adaptor proteins also interact with CD3ζ in TCR activated-, but not in resting-, T cells. Crk binding to CD3ζ was independent of ZAP70 and also occurred in ZAP70-deficient T cells. Binding was mediated by Crk-SH2 domain interaction with phosphotyrosine-containing motifs on CD3ζ, via a direct physical interaction, as demonstrated by Far-Western blot. CrkII binding to CD3ζ could also be demonstrated in a heterologous system, where coexpression of a catalytically active Lck was used to phosphorylate the CD3ζ chain. TCR activation-induced Crk binding to CD3ζ resulted in increased and prolonged phosphorylation of CD3ζ, as well as ZAP70 and LAT, suggesting a positive role for CrkI/II binding to CD3ζ in regulation of TCR-coupled signaling pathways. Furthermore, Crk-dependent increased phosphorylation of CD3ζ coincided with inhibition of TCR downmodulation, supporting a positive role for Crk adaptor proteins in TCR-mediated signal amplification. [Mh] Termos MeSH primário: Complexo CD3/metabolismo Regulação para Baixo Ativação Linfocitária Proteínas Proto-Oncogênicas c-crk/metabolismo Receptores de Antígenos de Linfócitos T/metabolismo Linfócitos T/metabolismo [Mh] Termos MeSH secundário: Animais Anticorpos/metabolismo Células COS Cercopithecus aethiops Reagentes para Ligações Cruzadas/farmacologia Regulação para Baixo/efeitos dos fármacos Seres Humanos Células Jurkat Ativação Linfocitária/efeitos dos fármacos Camundongos Peso Molecular Fosforilação/efeitos dos fármacos Fosfotirosina/metabolismo Ligação Proteica/efeitos dos fármacos Proteínas Proto-Oncogênicas c-crk/química Linfócitos T/efeitos dos fármacos Vanadatos/farmacologia Proteína-Tirosina Quinase ZAP-70/metabolismo Domínios de Homologia de src [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies); 0 (CD3 Complex); 0 (CRK protein, human); 0 (Cross-Linking Reagents); 0 (Proto-Oncogene Proteins c-crk); 0 (Receptors, Antigen, T-Cell); 0 (pervanadate); 21820-51-9 (Phosphotyrosine); 3WHH0066W5 (Vanadates); EC 2.7.10.2 (ZAP-70 Protein-Tyrosine Kinase); EC 2.7.10.2 (ZAP70 protein, human) [Em] Mês de entrada: 1803 [Cu] Atualização por classe: 180306 [Lr] Data última revisão: 180306 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170504 [St] Status: MEDLINE

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[PMID]: 28461105 [Au] Autor: Mavropoulos A; Varna A; Zafiriou E; Liaskos C; Alexiou I; Roussaki-Schulze A; Vlychou M; Katsiari C; Bogdanos DP; Sakkas LI [Ad] Endereço: Department of Rheumatology and Clinical Immunology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa 41 110, Greece. [Ti] Título: IL-10 producing Bregs are impaired in psoriatic arthritis and psoriasis and inversely correlate with IL-17- and IFNγ-producing T cells. [So] Source: Clin Immunol;184:33-41, 2017 11. [Is] ISSN: 1521-7035 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Our aim was to study CD19(+)CD27(+)CD24(high) memory and CD19(+)CD24(high)CD38(high) transitional and IL-10+Breg cells, known to inhibit Th1 and Th17 cells in experimental arthritis, in psoriatic arthritis (PsA) and psoriasis (Ps). Peripheral blood Breg cells from 60 patients with PsA, 50 patients with Ps and 23 healthy controls were analyzed by flow cytometry. IL-17A-producing CD3(+) T cells and IFNγ-producing CD3(+) T cells and activation of p38 MAPK and STAT3 were also studied. CD19(+)CD27(+)CD24(high) and CD19(+)CD24(high)CD38(high) Breg cells were decreased in PsA and Ps. In Ps patients, CD19(+)CD27(+)CD24(high) Breg cells inversely correlated with PASI score. IL-10+Bcells were also decreased and inversely correlated with IL-17A+CD3+ and IFN-γ+CD3+ T cells. B cells from patients exhibited impaired activation of p38 MAPK and STAT3. In conclusion, IL-10+Breg cells are decreased PsA and Ps and inversely correlated with the severity of psoriasis and IL-17A+ and IFNγ+ T cells. [Mh] Termos MeSH primário: Artrite Psoriásica/imunologia Linfócitos B Reguladores/imunologia Linfócitos T/imunologia [Mh] Termos MeSH secundário: Adulto Idoso Antirreumáticos/uso terapêutico Artrite Psoriásica/tratamento farmacológico Artrite Psoriásica/metabolismo Complexo CD3/imunologia Feminino Citometria de Fluxo Seres Humanos Interferon gama/imunologia Interleucina-10/imunologia Interleucina-17/imunologia Masculino Meia-Idade Psoríase/tratamento farmacológico Psoríase/imunologia Psoríase/metabolismo Fator de Transcrição STAT3/metabolismo Índice de Gravidade de Doença Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antirheumatic Agents); 0 (CD3 Complex); 0 (IFNG protein, human); 0 (IL10 protein, human); 0 (Interleukin-17); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 130068-27-8 (Interleukin-10); 82115-62-6 (Interferon-gamma); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 180206 [Lr] Data última revisão: 180206 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170503 [St] Status: MEDLINE

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[PMID]: 28743717 [Au] Autor: Blázquez-Moreno A; Pérez-Portilla A; Agúndez-Llaca M; Dukovska D; Valés-Gómez M; Aydogmus C; Ikinciogullari A; Regueiro JR; Reyburn HT [Ad] Endereço: Department of Immunology and Oncology, National Center for Biotechnology and Spanish National Research Council, Madrid, Spain. [Ti] Título: Analysis of the recovery of CD247 expression in a PID patient: insights into the spontaneous repair of defective genes. [So] Source: Blood;130(10):1205-1208, 2017 09 07. [Is] ISSN: 1528-0020 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Mutations in T-cell antigen receptor (TCR) subunit genes cause rare immunodeficiency diseases characterized by impaired expression of the TCR at the cell surface and selective T lymphopenia. Here, detailed analyses of spontaneously arising somatic mutations that recover CD247, and thus TCR expression, in a newly identified CD247-deficient patient are described. The recovery of CD247 expression in some patient T cells was associated with both reversion of the inactivating mutation and a variant with a compensating mutation that could reconstitute TCR expression, but not as efficiently as wild-type CD247. Multiple mutations were found in CD247 complementary DNAs (cDNAs) cloned from the patient as well as in cDNA and genomic DNA from other individuals, suggesting that genetic variation in this gene is frequent. Analyses of other genes mutated in primary immunodeficiency diseases (PIDs) where reversions have been described also revealed a higher rate of mutation than that observed for genes mutated in PIDs where revertants have not been identified or control genes. These data support the hypothesis that the occurrence of somatic mutations that may reconstitute genetic defects in PID is related to an increased propensity of those genes to mutate. [Mh] Termos MeSH primário: Complexo CD3/genética Reparo do DNA/genética Regulação da Expressão Gênica Síndromes de Imunodeficiência/genética [Mh] Termos MeSH secundário: Seres Humanos Leucócitos Mononucleares/metabolismo Mutação/genética Probabilidade [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (CD3 Complex); 0 (CD3 antigen, zeta chain) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 180113 [Lr] Data última revisão: 180113 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170727 [St] Status: MEDLINE [do] DOI: 10.1182/blood-2017-01-762864

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[PMID]: 29017923 [Au] Autor: Shinjo Y; Makide K; Satoh K; Fukami F; Inoue A; Kano K; Otani Y; Ohwada T; Aoki J [Ad] Endereço: Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Miyagi 980-8578, Japan. [Ti] Título: Lysophosphatidylserine suppresses IL-2 production in CD4 T cells through LPS /GPR174. [So] Source: Biochem Biophys Res Commun;494(1-2):332-338, 2017 Dec 09. [Is] ISSN: 1090-2104 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Lysophosphatidylserine (LysoPS) has been shown to have lipid mediator-like actions to induce mast cell degranulation and suppress T lymphocyte proliferation. Recently, three G protein-coupled receptors (GPCRs), LPS /GPR34, LPS /P2Y10, and LPS /GPR174, were found to react specifically with LysoPS, raising the possibility that LysoPS exerts its roles through these receptors. In this study, we show that LPS is expressed in various T cell subtypes and is involved in suppression of Interleukin-2 (IL-2) production in CD4 T cells. We found that LysoPS suppressed the IL-2 production from activated T cells at the mRNA and protein levels. In addition, LysoPS did not have such an effect on the splenocytes and CD4 T cells isolated from LPS -deficient mice. In LPS -deficient splenocytes and CD4 T cells, anti-CD3/anti-CD28-triggered IL-2 production is somewhat increased. Interestingly, LysoPS with various fatty acids was up-regulated upon T cell activation. The present study raised the possibility that LysoPS exerts its immunosuppressive roles by down-regulating IL-2 production through a LysoPS-LPS axis in T cells. [Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/efeitos dos fármacos Interleucina-2/genética Lisofosfolipídeos/farmacologia Receptores Acoplados a Proteínas-G/genética Receptores de Lisofosfolipídeos/genética Receptores Purinérgicos P2/genética [Mh] Termos MeSH secundário: Animais Anticorpos/farmacologia Antígenos CD28/antagonistas & inibidores Antígenos CD28/genética Antígenos CD28/imunologia Complexo CD3/genética Complexo CD3/imunologia Linfócitos T CD4-Positivos/citologia Linfócitos T CD4-Positivos/imunologia Separação Celular Regulação da Expressão Gênica Interleucina-2/imunologia Lisofosfolipídeos/imunologia Camundongos Camundongos Endogâmicos BALB C Camundongos Endogâmicos C57BL Cultura Primária de Células Receptores Acoplados a Proteínas-G/imunologia Receptores de Lisofosfolipídeos/imunologia Receptores Purinérgicos P2/imunologia Transdução de Sinais Baço/citologia Baço/efeitos dos fármacos Baço/imunologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies); 0 (CD28 Antigens); 0 (CD3 Complex); 0 (G-protein-coupled receptor 34); 0 (GPR174 protein, mouse); 0 (Interleukin-2); 0 (Lysophospholipids); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Lysophospholipid); 0 (Receptors, Purinergic P2); 0 (lysophosphatidylserine) [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: 171012 [St] Status: MEDLINE

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[PMID]: 28975663 [Au] Autor: Ryu HJ; Kim EK; Heo SJ; Cho BC; Kim HR; Yoon SO [Ad] Endereço: Department of Pathology, Yonsei University College of Medicine, Seoul, Korea. [Ti] Título: Architectural patterns of p16 immunohistochemical expression associated with cancer immunity and prognosis of head and neck squamous cell carcinoma. [So] Source: APMIS;125(11):974-984, 2017 Nov. [Is] ISSN: 1600-0463 [Cp] País de publicação: Denmark [La] Idioma: eng [Ab] Resumo: We evaluated the expression patterns of p16, which is used as a surrogate marker of HPV infection in head and neck squamous cell carcinoma (HNSCC), in regard to their biological and prognostic implications. p16 expression patterns and infiltrated immune cells were analyzed through immunohistochemistry of p16, CD3, CD8, PD-1, FOXP3, and CD163 on surgically resected HNSCCs (n = 393). Patterns of p16 immunoexpression were defined as STRONG (strong, diffuse expression in cytoplasm, and nucleus in >70% of tumor cells), MARGINAL (expression restricted to tumor margins), MOSAIC (ragged, discontinued expression), NUCLEAR (expression in nuclei only), and ABSENT (no expression). The STRONG pattern was more frequent in the oropharynx, and the MARGINAL pattern was noted only in the oral cavity. MOSAIC and NUCLEAR patterns were noted at variable sites. No two patterns of p16 expression showed the same immune cell composition of CD3+ T cells, CD8+ cytotoxic T cells, PD-1+ T cells, FOXP3+ regulatory T cells, and CD163+ macrophages. In overall and disease-free survival analyses, the STRONG pattern showed the most favorable prognosis, while the NUCLEAR pattern had the worst prognosis. HNSCC anatomical sites, tumor-related immune cell components, and patient outcomes were associated with p16 expression patterns. Each architectural pattern of p16 expression may be related to different biological and prognostic phenotypes. [Mh] Termos MeSH primário: Biomarcadores Tumorais/genética Carcinoma de Células Escamosas/diagnóstico Inibidor p16 de Quinase Dependente de Ciclina/genética Neoplasias de Cabeça e Pescoço/diagnóstico Infecções por Papillomavirus/diagnóstico [Mh] Termos MeSH secundário: Idoso Antígenos CD/genética Antígenos CD/imunologia Antígenos de Diferenciação Mielomonocítica/genética Antígenos de Diferenciação Mielomonocítica/imunologia Biomarcadores Tumorais/imunologia Complexo CD3/genética Complexo CD3/imunologia Antígenos CD8/genética Antígenos CD8/imunologia Carcinoma de Células Escamosas/genética Carcinoma de Células Escamosas/mortalidade Carcinoma de Células Escamosas/patologia Inibidor p16 de Quinase Dependente de Ciclina/imunologia Feminino Fatores de Transcrição Forkhead/genética Fatores de Transcrição Forkhead/imunologia Expressão Gênica Neoplasias de Cabeça e Pescoço/genética Neoplasias de Cabeça e Pescoço/mortalidade Neoplasias de Cabeça e Pescoço/patologia Papillomavirus Humano 16/crescimento & desenvolvimento Papillomavirus Humano 16/patogenicidade Seres Humanos Masculino Meia-Idade Infecções por Papillomavirus/genética Infecções por Papillomavirus/mortalidade Infecções por Papillomavirus/patologia Prognóstico Receptor de Morte Celular Programada 1/genética Receptor de Morte Celular Programada 1/imunologia Receptores de Superfície Celular/genética Receptores de Superfície Celular/imunologia Análise de Sobrevida [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Biomarkers, Tumor); 0 (CD163 antigen); 0 (CD3 Complex); 0 (CD8 Antigens); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (P16 protein, human); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Cell Surface) [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: 171005 [St] Status: MEDLINE [do] DOI: 10.1111/apm.12744

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[PMID]: 28922848 [Au] Autor: Richardson TE; Shen ZJ; Kanchwala M; Xing C; Filatenkov A; Shang P; Barnett S; Abedin Z; Malter JS; Raisanen JM; Burns DK; White CL; Hatanpaa KJ [Ad] Endereço: Department of Pathology; Eugene McDermott Center for Human Growth and Development; Department of Bioinformatics; Department of Clinical Sciences and Department of Neurosurgery, University of Texas Southwestern Medical Center, Dallas, Texas; PrimBio Research Institute, LLC, Exton, Pennsylvania. [Ti] Título: Aggressive Behavior in Silent Subtype III Pituitary Adenomas May Depend on Suppression of Local Immune Response: A Whole Transcriptome Analysis. [So] Source: J Neuropathol Exp Neurol;76(10):874-882, 2017 Oct 01. [Is] ISSN: 1554-6578 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Silent subtype III pituitary adenomas (SS-3) are clinically nonfunctional adenomas that are more aggressive in terms of invasion and risk of recurrence than their conventional null cell counterparts. We previously showed that these tumors can be distinguished by immunohistochemistry based on the identification of a markedly enlarged and fragmented Golgi apparatus. To understand the molecular correlates of differential aggressiveness, we performed whole transcriptome sequencing (RNAseq) on 4 SS-3 and 4 conventional null cell adenomas. The genes that were highly upregulated in all the SS-3 adenomas included 2 secreted proteins involved in the suppression of T-lymphocyte activity, i.e., ARG2 (multiple testing adjusted padj = 1.5 × 10-3) and SEMA3A (padj = 3.3 × 10-3). Highly downregulated genes in all the SS-3 adenomas included HLA-B (padj = 3.3 × 10-6), suggesting reduced antigen presentation by the adenoma to cytotoxic T-cells. Quantitative RT-PCR of these genes performed on the adenoma samples supported the RNAseq results. We also found a relative decrease in the overall concentration of T-lymphocytes in the SS-3 tumors. These results suggest that SS-3 adenomas actively suppress the immune system and raise the possibility that they may be treatable with immune checkpoint inhibitors or nonspecific cancer immunotherapies. [Mh] Termos MeSH primário: Adenoma Agressão/fisiologia Imunidade Inata Linfócitos/patologia Neoplasias Hipofisárias [Mh] Termos MeSH secundário: Adenoma/genética Adenoma/imunologia Adenoma/fisiopatologia Adulto Idoso Arginase/genética Arginase/metabolismo Complexo CD3/metabolismo Feminino Expressão Gênica Perfilação da Expressão Gênica Antígenos HLA-B/genética Antígenos HLA-B/metabolismo Seres Humanos Linfócitos/metabolismo Masculino Meia-Idade Proteínas de Neoplasias/genética Proteínas de Neoplasias/metabolismo Neoplasias Hipofisárias/genética Neoplasias Hipofisárias/imunologia Neoplasias Hipofisárias/fisiopatologia RNA Mensageiro/metabolismo Estudos Retrospectivos Semaforina-3A/genética Semaforina-3A/metabolismo Transdução de Sinais/genética [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (CD3 Complex); 0 (HLA-B Antigens); 0 (Neoplasm Proteins); 0 (RNA, Messenger); 0 (SEMA3A protein, human); 0 (Semaphorin-3A); EC 3.5.3.1 (Arginase); EC 3.5.3.1 (arginase II, human) [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: 170920 [St] Status: MEDLINE [do] DOI: 10.1093/jnen/nlx072

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MEDLINE

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[PMID]: 28846388 [Au] Autor: Hammink R; Eggermont LJ; Zisis T; Tel J; Figdor CG; Rowan AE; Blank KG [Ad] Endereço: Department of Molecular Materials, Institute for Molecules and Materials, Radboud University , Heyendaalseweg 135, 6525 AJ Nijmegen, The Netherlands. [Ti] Título: Affinity-Based Purification of Polyisocyanopeptide Bioconjugates. [So] Source: Bioconjug Chem;28(10):2560-2568, 2017 Oct 18. [Is] ISSN: 1520-4812 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Water-soluble polyisocyanopeptides (PICs) are a new class of synthetic polymers that mimic natural protein-based filaments. Their unique semiflexible properties combined with a length of several hundred nanometers have recently enabled a number of biomedical applications ranging from tissue engineering to cancer immunotherapy. One crucial step toward the further development of PICs for these applications is the efficient and controlled synthesis and purification of PIC-biomolecule conjugates. Considering the large size of PICs and the biomolecules to be conjugated, conjugation reactions do usually not proceed to completion due to steric effects. As a consequence, purification of the reaction mixture is necessary to separate the obtained bioconjugates from unreacted biomolecules. As a direct result of the semiflexible nature of PICs, standard polymer and protein purification methods based on molecular weight have not been successful. Here, we introduce a new affinity-based purification method utilizing biotin as an affinity tag. PICs decorated with a controlled and tunable density of biotin molecules (biotinPICs) were efficiently bound to and eluted from a monoavidin resin in buffered aqueous solution. Using these biotinPICs, two different protein conjugates were synthesized, one carrying the enzyme alkaline phosphatase (PhoA) and the other T-cell activating anti-CD3 antibodies. The resulting biotinPIC-protein conjugates were successfully obtained in high purity (>90%) and without any loss of protein activity. The high purity greatly simplifies the analysis of biotinPIC bioconjugates, such as the determination of the average number of biomolecules conjugated per biotinPIC chain. Most importantly, it allows for the direct and straightforward application of the obtained bioconjugates in the desired applications. The new method developed may further be adapted for the purification of other advanced bioconjugates that are difficult to obtain in high purity with the available standard methods. [Mh] Termos MeSH primário: Dipeptídeos/química Dipeptídeos/isolamento & purificação Nitrilos/química Nitrilos/isolamento & purificação [Mh] Termos MeSH secundário: Fosfatase Alcalina/metabolismo Animais Anticorpos Monoclonais/química Anticorpos Monoclonais/imunologia Avidina/química Avidina/metabolismo Biotina/química Complexo CD3/imunologia Escherichia coli/enzimologia Seres Humanos Imunoconjugados/química Imunoconjugados/isolamento & purificação Solubilidade Água/química [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antibodies, Monoclonal); 0 (CD3 Complex); 0 (Dipeptides); 0 (Immunoconjugates); 0 (Nitriles); 0 (poly(isocyanodipeptide)); 059QF0KO0R (Water); 1405-69-2 (Avidin); 6SO6U10H04 (Biotin); EC 3.1.3.1 (Alkaline Phosphatase) [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: 170829 [St] Status: MEDLINE [do] DOI: 10.1021/acs.bioconjchem.7b00398

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MEDLINE

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[PMID]: 28844471 [Au] Autor: Long SA; Thorpe J; Herold KC; Ehlers M; Sanda S; Lim N; Linsley PS; Nepom GT; Harris KM [Ad] Endereço: Benaroya Research Institute at Virginia Mason, Seattle, WA, USA. [Ti] Título: Remodeling T cell compartments during anti-CD3 immunotherapy of type 1 diabetes. [So] Source: Cell Immunol;319:3-9, 2017 Sep. [Is] ISSN: 1090-2163 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: The immunological mechanism(s) of action whereby teplizumab preserves C-peptide levels in the progression of patients with recent onset type 1 diabetes (T1D) is still not well understood. In the present study, we evaluated the kinetics of T cell modulation in peripheral blood following two 14-day courses of teplizumab therapy one year apart in recent onset T1D participants in the AbATE clinical trial. Transient rises in PD-1+Foxp3+ Treg and potentially anergic (CD57-KLRG1-PD-1+) cells in the circulating CD4 T cell compartment were paralleled by more profound increases in circulating CD8 T cells with traits of exhaustion (CD57-KLRG1+PD-1+, TIGIT+KLRG1+, and persistent down-modulation of CD127). The observed phenotypic changes across cell types were associated with favorable response to treatment in the subgroup of study participants that did not develop anti-drug antibodies after the first course of therapy. These findings provide new insights on the duration and complexity of T cell modulation with teplizumab therapy in recent onset T1D, and in addition, suggest that coordinated immune mechanisms of tolerance that favor CD4 Treg function and restrain CD4 non-Treg and CD8 T cell activation may contribute to treatment success. [Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico Linfócitos T CD8-Positivos/efeitos dos fármacos Diabetes Mellitus Tipo 1/tratamento farmacológico Hipoglicemiantes/uso terapêutico Tolerância Imunológica/efeitos dos fármacos Linfócitos T Reguladores/efeitos dos fármacos [Mh] Termos MeSH secundário: Adolescente Adulto Peptídeo C/agonistas Peptídeo C/genética Peptídeo C/imunologia Complexo CD3/genética Complexo CD3/imunologia Antígenos CD57/genética Antígenos CD57/imunologia Linfócitos T CD8-Positivos/imunologia Linfócitos T CD8-Positivos/patologia Criança Diabetes Mellitus Tipo 1/imunologia Diabetes Mellitus Tipo 1/patologia Feminino Fatores de Transcrição Forkhead/genética Fatores de Transcrição Forkhead/imunologia Expressão Gênica Seres Humanos Imunomodulação Imunoterapia/métodos Subunidade alfa de Receptor de Interleucina-7/genética Subunidade alfa de Receptor de Interleucina-7/imunologia Lectinas Tipo C/genética Lectinas Tipo C/imunologia Masculino Receptor de Morte Celular Programada 1/genética Receptor de Morte Celular Programada 1/imunologia Receptores Imunológicos/genética Receptores Imunológicos/imunologia Linfócitos T Reguladores/imunologia Linfócitos T Reguladores/patologia Transativadores/genética Transativadores/imunologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL [Nm] Nome de substância: 0 (Antibodies, Monoclonal, Humanized); 0 (C-Peptide); 0 (CD3 Complex); 0 (CD57 Antigens); 0 (FOXP3 protein, human); 0 (Forkhead Transcription Factors); 0 (Hypoglycemic Agents); 0 (Interleukin-7 Receptor alpha Subunit); 0 (KLRG1 protein, human); 0 (Lectins, C-Type); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (TIGIT protein, human); 0 (Trans-Activators); S4M959U2IJ (teplizumab) [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: 170829 [St] Status: MEDLINE

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