Base de dados : MEDLINE Pesquisa : D23.050.301.264.894.108 [Categoria DeCS] Referências encontradas : 8510 [refinar] Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 851

ir para página

1 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 28922790 [Au] Autor: Marisa L; Svrcek M; Collura A; Becht E; Cervera P; Wanherdrick K; Buhard O; Goloudina A; Jonchère V; Selves J; Milano G; Guenot D; Cohen R; Colas C; Laurent-Puig P; Olschwang S; Lefèvre JH; Parc Y; Boige V; Lepage C; André T; Fléjou JF; Dérangère V; Ghiringhelli F; de Reynies A; Duval A [Ad] Endereço: Programme "Cartes d'Identité des Tumeurs," Ligue Nationale Contre le Cancer, Paris, France; INSERM, UMRS 938 - Centre de Recherche Saint-Antoine, Equipe "Instabilité des Microsatellites et Cancers," Equipe labellisée par la Ligue Nationale contre le Cancer, Paris, France; Sorbonne Université, UPMC U [Ti] Título: The Balance Between Cytotoxic T-cell Lymphocytes and Immune Checkpoint Expression in the Prognosis of Colon Tumors. [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: Immune checkpoint (ICK) expression might represent a surrogate measure of tumor-infiltrating T cell (CTL) exhaustion and therefore be a more accurate prognostic biomarker for colorectal cancer (CRC) patients than CTL enumeration as measured by the Immunoscore. Methods: The expression of ICKs, Th1, CTLs, cytotoxicity-related genes, and metagenes, including Immunoscore-like metagenes, were evaluated in three independent cohorts of CRC samples (260 microsatellite instable [MSI], 971 non-MSI). Their associations with patient survival were analyzed by Cox models, taking into account the microsatellite instability (MSI) status and affiliation with various Consensus Molecular Subgroups (CMS). PD-L1 and CD8 expression were examined on a subset of tumors with immunohistochemistry. All statistical tests were two-sided. Results: The expression of Immunoscore-like metagenes was statistically significantly associated with improved outcome in non-MSI tumors displaying low levels of both CTLs and immune checkpoints (ICKs; CMS2 and CMS3; hazard ratio [HR] = 0.63, 95% confidence interval [CI] = 0.43 to 0.92, P = .02; and HR = 0.55, 95% CI = 0.34 to 0.90, P = .02, respectively), but clearly had no prognostic relevance in CRCs displaying higher levels of CTLs and ICKs (CMS1 and CMS4; HR = 0.46, 95% CI = 0.10 to 2.10, P = .32; and HR = 1.13, 95% CI = 0.79 to 1.63, P = .50, respectively), including MSI tumors. ICK metagene expression was statistically significantly associated with worse prognosis independent of tumor staging in MSI tumors (HR = 3.46, 95% CI = 1.41 to 8.49, P = .007). ICK expression had a negative impact on the proliferation of infiltrating CD8 T cells in MSI neoplasms (median = 0.56 in ICK low vs median = 0.34 in ICK high, P = .004). Conclusions: ICK expression cancels the prognostic relevance of CTLs in highly immunogenic colon tumors and predicts a poor outcome in MSI CRC patients. [Mh] Termos MeSH primário: Biomarcadores Tumorais/genética Biomarcadores Tumorais/imunologia Neoplasias Colorretais/genética Neoplasias Colorretais/imunologia Linfócitos do Interstício Tumoral Linfócitos T Citotóxicos [Mh] Termos MeSH secundário: Antígenos CD/genética Antígeno B7-H1/análise Antígeno B7-H1/genética Antígenos CD8/análise Antígeno CTLA-4/genética Colo/química Neoplasias Colorretais/química Neoplasias Colorretais/patologia Feminino Expressão Gênica Receptor Celular 2 do Vírus da Hepatite A/genética Seres Humanos Proteína Coestimuladora de Linfócitos T Induzíveis/genética Masculino Instabilidade de Microssatélites Meia-Idade Estadiamento de Neoplasias Prognóstico Proteína 2 Ligante de Morte Celular Programada 1/genética Receptor de Morte Celular Programada 1/genética Estudos Retrospectivos Taxa de Sobrevida Células Th1 [Pt] Tipo de publicação: JOURNAL ARTICLE; MULTICENTER STUDY [Nm] Nome de substância: 0 (Antigens, CD); 0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD223 antigen); 0 (CD274 protein, human); 0 (CD8 Antigens); 0 (CTLA-4 Antigen); 0 (HAVCR2 protein, human); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (ICOS protein, human); 0 (Inducible T-Cell Co-Stimulator Protein); 0 (PDCD1 protein, human); 0 (PDCD1LG2 protein, human); 0 (Programmed Cell Death 1 Ligand 2 Protein); 0 (Programmed Cell Death 1 Receptor) [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/djx136

2 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 29324830 [Au] Autor: Skeate JG; Da Silva DM; Chavez-Juan E; Anand S; Nuccitelli R; Kast WM [Ad] Endereço: Department of Molecular Microbiology & Immunology, University of Southern California, Los Angeles, CA, United States of America. [Ti] Título: Nano-Pulse Stimulation induces immunogenic cell death in human papillomavirus-transformed tumors and initiates an adaptive immune response. [So] Source: PLoS One;13(1):e0191311, 2018. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Nano-Pulse Stimulation (NPS) is a non-thermal pulsed electric field modality that has been shown to have cancer therapeutic effects. Here we applied NPS treatment to the human papillomavirus type 16 (HPV 16)-transformed C3.43 mouse tumor cell model and showed that it is effective at eliminating primary tumors through the induction of immunogenic cell death while subsequently increasing the number of tumor-infiltrating lymphocytes within the tumor microenvironment. In vitro NPS treatment of C3.43 cells resulted in a doubling of activated caspase 3/7 along with the translocation of phosphatidylserine (PS) to the outer leaflet of the plasma membrane, indicating programmed cell death activity. Tumor-bearing mice receiving standard NPS treatment showed an initial decrease in tumor volume followed by clearing of tumors in most mice, and a significant increase in overall survival. Intra-tumor analysis of mice that were unable to clear tumors showed an inverse correlation between the number of tumor infiltrating lymphocytes and the size of the tumor. Approximately half of the mice that cleared established tumors were protected against tumor re-challenge on the opposite flank. Selective depletion of CD8+ T cells eliminated this protection, suggesting that NPS treatment induces an adaptive immune response generating CD8+ T cells that recognize tumor antigen(s) associated with the C3.43 tumor model. This method may be utilized in the future to not only ablate primary tumors, but also to induce an anti-tumor response driven by effector CD8+ T cells capable of protecting individuals from disease recurrence. [Mh] Termos MeSH primário: Imunidade Adaptativa Morte Celular/imunologia Transformação Celular Viral Estimulação Elétrica Papillomavirus Humano 16/fisiologia [Mh] Termos MeSH secundário: Animais Antígenos CD8/metabolismo Caspase 3/metabolismo Caspase 7/metabolismo Linhagem Celular Tumoral Ativação Enzimática Seres Humanos Camundongos Nanotecnologia Carga Tumoral [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (CD8 Antigens); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 7) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180226 [Lr] Data última revisão: 180226 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180112 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0191311

3 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 29304116 [Au] Autor: Lange A; Jaskula E; Lange J; Dworacki G; Nowak D; Simiczyjew A; Mordak-Domagala M; Sedzimirska M [Ad] Endereço: L. Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland. [Ti] Título: The sorafenib anti-relapse effect after alloHSCT is associated with heightened alloreactivity and accumulation of CD8+PD-1+ (CD279+) lymphocytes in marrow. [So] Source: PLoS One;13(1):e0190525, 2018. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: We studied three FLT3 ITD acute myeloid leukemia (AML) patients who relapsed after allogeneic haematopoietic stem cell transplantation (alloHSCT) and received multikinase inhibitor (MKI) sorafenib as part of salvage therapy. MKI was given to block the effect of FLT3 ITD mutation which powers proliferation of blast cells. However, the known facts that sorafenib is more effective in patents post alloHSCT suggested that this MKI can augment the immune system surveillance on leukaemia. In the present study, we investigated in depth the effect of sorafenib on the alloreactivity seen post-transplant including that on leukaemia. The patients (i) responded to the treatment with cessation of blasts which lasted 1, 17 and 42+ months, (ii) developed skin lesions with CD3+ cell invasion of the epidermis, (iii) had marrow infiltrated with CD8+ lymphocytes which co-expressed PD-1 (programmed cell death protein 1 receptor, CD279) in higher proportions than those in the blood (163±32 x103 cells/µl vs 38±8 x103 cells/µl, p<0.001). The Lymphoprep fraction of marrow cells investigated for the expression of genes involved in lymphocyte activation showed in the patients with long lasting complete remission (CR) a similar pattern characterized by (i) a low expression of nitric oxide synthase 2 (NOS2) and colony stimulating factor 2 (CSF2) as well as that of angiopoietin-like 4 (ANGPTL4) (supporting the immune response and anti-angiogenic) genes, and (ii) higher expression of fibroblast growth factor 1 (FGF1) and collagen type IV alpha 3 chain (COL4A3) as well as toll like receptor 9 (TLR9) and interleukin-12 (IL-12) (pro-inflammatory expression profile) genes as compared with the normal individual. The positive effect in one patient hardly justified the presence of unwanted effects (progressive chronic graft-versus-host disease (cGvHD) and avascular necrosis of the femur), which were in contrast negligible in the other patient. The anti-leukemic and unwanted effects of sorafenib do not rely on each other. [Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico Células da Medula Óssea/imunologia Antígenos CD8/imunologia Transplante de Células-Tronco Hematopoéticas/efeitos adversos Leucemia Mieloide Aguda/cirurgia Linfócitos/imunologia Niacinamida/análogos & derivados Compostos de Fenilureia/uso terapêutico Receptor de Morte Celular Programada 1/imunologia [Mh] Termos MeSH secundário: Feminino Seres Humanos Leucemia Mieloide Aguda/imunologia Masculino Meia-Idade Niacinamida/uso terapêutico Recidiva Transplante Homólogo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (CD8 Antigens); 0 (PDCD1 protein, human); 0 (Phenylurea Compounds); 0 (Programmed Cell Death 1 Receptor); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib) [Em] Mês de entrada: 1802 [Cu] Atualização por classe: 180215 [Lr] Data última revisão: 180215 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180106 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0190525

4 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 29342151 [Au] Autor: Boddaert J; Bielen K; 's Jongers B; Manocha E; Yperzeele L; Cras P; Pirici D; Kumar-Singh S [Ad] Endereço: Molecular Pathology Group, Cell Biology and Histology, Faculty of Medicine and Health Sciences, Wilrijk, Belgium. [Ti] Título: CD8 signaling in microglia/macrophage M1 polarization in a rat model of cerebral ischemia. [So] Source: PLoS One;13(1):e0186937, 2018. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Classical or M1 activity of microglia/macrophages has been described in several neurodegenerative and brain inflammatory conditions and has also been linked to expansion of ischemic injury in post-stroke brain. While different pathways of M1 polarization have been suggested to occur in the post-stroke brain, the precise underlying mechanisms remain undefined. Using a transient middle cerebral artery occlusion (MCAO) rat model, we showed a progressive M2 to M1 polarization in the perilesional brain region with M1 cells becoming one of the dominant subsets by day 4 post-stroke. Comparing key receptors involved in M1 polarization (CD8, IFNγR, Clec4, FcγR, TLR3 and TLR4) and their signal transducers (Syk, Stat1, Irf3, and Traf6) at the day 4 time point, we showed a strong upregulation of CD8 along with SYK transducer in dissected perilesional brain tissue. We further showed that CD8 expression in the post-stroke brain was associated with activated (CD68+) macrophages and that progressive accumulation of CD8+CD68+ cells in the post-stroke brain coincided with increased iNOS (M1 marker) and reduced Arg1 (M2 marker) expression on these cells. In vitro ligand-based stimulation of the CD8 receptor caused increased iNOS expression and an enhanced capacity to phagocytose E. coli particles; and interestingly, CD8 stimulation was also able to repolarize IL4-treated M2 cells to an M1 phenotype. Our data suggest that increased CD8 signaling in the post-stroke brain is primarily associated with microglia/macrophages and can independently drive M1 polarization, and that modulation of CD8 signaling could be a potential target to limit secondary post-stroke brain damage. [Mh] Termos MeSH primário: Isquemia Encefálica/metabolismo Antígenos CD8/metabolismo Polaridade Celular Macrófagos/metabolismo Microglia/metabolismo [Mh] Termos MeSH secundário: Animais Modelos Animais de Doenças Feminino Masculino Ratos Ratos Wistar [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (CD8 Antigens) [Em] Mês de entrada: 1801 [Cu] Atualização por classe: 180210 [Lr] Data última revisão: 180210 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 180118 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0186937

5 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 28468970 [Au] Autor: Chowdhary VR; Krogman A; Tilahun AY; Alexander MP; David CS; Rajagopalan G [Ad] Endereço: Division of Rheumatology, Department of Medicine, Mayo Clinic, Rochester, MN 55905. [Ti] Título: Concomitant Disruption of and Genes Facilitates the Development of Double Negative αß TCR Peripheral T Cells That Respond Robustly to Staphylococcal Superantigen. [So] Source: J Immunol;198(11):4413-4424, 2017 06 01. [Is] ISSN: 1550-6606 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Mature peripheral double negative T (DNT) cells expressing αß TCR but lacking CD4/CD8 coreceptors play protective as well as pathogenic roles. To better understand their development and functioning in vivo, we concomitantly inactivated and genes in mice with intact MHC class I and class II molecules with the hypothesis that this would enable the development of DNT cells. We also envisaged that these DNT cells could be activated by bacterial superantigens in vivo as activation of T cells by superantigens does not require CD4 and CD8 coreceptors. Because HLA class II molecules present superantigens more efficiently than murine MHC class II molecules, CD4 CD8 double knockout (DKO) mice transgenically expressing HLA-DR3 or HLA-DQ8 molecules were generated. Although thymic cellularity was comparable between wild type (WT) and DKO mice, CD3 αß TCR thymocytes were significantly reduced in DKO mice, implying defects in thymic-positive selection. Splenic CD3 αß TCR cells and Foxp3 T regulatory cells were present in DKO mice but significantly reduced. However, the in vivo inflammatory responses and immunopathology elicited by acute challenge with the staphylococcal superantigen enterotoxin B were comparable between WT and DKO mice. Choric exposure to staphylococcal enterotoxin B precipitated a lupus-like inflammatory disease with characteristic lympho-monocytic infiltration in lungs, livers, and kidneys, along with production of anti-nuclear Abs in DKO mice as in WT mice. Overall, our results suggest that DNT cells can develop efficiently in vivo and chronic exposure to bacterial superantigens may precipitate a lupus-like autoimmune disease through activation of DNT cells. [Mh] Termos MeSH primário: Antígenos CD4/genética Antígenos CD4/imunologia Antígenos CD8/genética Antígenos CD8/imunologia Enterotoxinas/imunologia Superantígenos/imunologia Subpopulações de Linfócitos T/imunologia [Mh] Termos MeSH secundário: Animais Antígenos HLA-DQ/genética Antígenos HLA-DQ/imunologia Antígeno HLA-DR3/genética Antígeno HLA-DR3/imunologia Antígenos de Histocompatibilidade Classe II/imunologia Camundongos Camundongos Knockout Camundongos Transgênicos Receptores de Antígenos de Linfócitos T alfa-beta/genética Receptores de Antígenos de Linfócitos T alfa-beta/imunologia Baço/citologia Baço/imunologia Timo/citologia Timo/imunologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL [Nm] Nome de substância: 0 (CD4 Antigens); 0 (CD8 Antigens); 0 (Enterotoxins); 0 (HLA-DQ Antigens); 0 (HLA-DQ8 antigen); 0 (HLA-DR3 Antigen); 0 (Histocompatibility Antigens Class II); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Superantigens); 39424-53-8 (enterotoxin B, staphylococcal) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 180127 [Lr] Data última revisão: 180127 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170505 [St] Status: MEDLINE [do] DOI: 10.4049/jimmunol.1601991

6 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 29083052 [Au] Autor: Erazo-Borrás LV; Álvarez-Álvarez JA; Perez-Romero CA; Orrego-Arango JC; Franco-Restrepo JL; Trujillo-Vargas CM [Ad] Endereço: Grupo de Inmunodeficiencias Primarias, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia. [Ti] Título: Skewed Invariant Natural Killer T (iNKT) Cells, Impaired iNKT:B Cell Help and Decreased SAP Expression in Blood Lymphocytes from Patients with Common Variable Immunodeficiency. [So] Source: Scand J Immunol;86(3):171-178, 2017 Sep. [Is] ISSN: 1365-3083 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: Common variable immunodeficiency (CVID) is a syndrome with predominantly defective B cell function. However, abnormalities in the number and function of other lymphocyte subpopulations in peripheral blood (PB) have been described in most patients. We have analysed the distribution of iNKT cell subpopulations in the PB of CVID patients and the ability of these cells to provide in vitro cognate B cell help. The total of iNKT cells was reduced in the PB of CVID patients, especially CD4+, CD4-/CD8- and CCR5+/CXCR3+. These findings were associated with an enrichment of memory-like and a tendency towards a reduction in TNF-α-expressing effector iNKT cells in the peripheral blood mononuclear cells (PBMC) of CVID patients. Moreover, an accumulation of follicular helper iNKT cells in the PB of CVID patients was demonstrated. CVID αGalCer-pulsed iNKT cells are not able to induce autologous B cell proliferation although they do induce proliferation to healthy donor B cells. Interestingly, autologous and heterologous co-cultures did not differ in the amount of immunoglobulin secreted by B cells in vitro. Finally, reduced intracellular SAP expression in iNKT cells and other lymphocytes in the blood from CVID patients was observed. These results provide further insights into the immunological mechanisms underlying the iNKT cell defects and the potential targets to improve B cell help in CVID. [Mh] Termos MeSH primário: Linfócitos B/imunologia Comunicação Celular Imunodeficiência de Variável Comum/imunologia Células T Matadoras Naturais/imunologia Saposinas/metabolismo [Mh] Termos MeSH secundário: Adolescente Adulto Antígenos CD4/metabolismo Antígenos CD8/metabolismo Proliferação Celular Células Cultivadas Técnicas de Cocultura Feminino Galactosilceramidas/imunologia Seres Humanos Imunoglobulinas/metabolismo Memória Imunológica Ativação Linfocitária Masculino Meia-Idade Receptores CCR5/metabolismo Receptores CXCR3/metabolismo Fator de Necrose Tumoral alfa/metabolismo Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (CCR5 protein, human); 0 (CD4 Antigens); 0 (CD8 Antigens); 0 (CXCR3 protein, human); 0 (Galactosylceramides); 0 (Immunoglobulins); 0 (PSAP protein, human); 0 (Receptors, CCR5); 0 (Receptors, CXCR3); 0 (Saposins); 0 (Tumor Necrosis Factor-alpha) [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: 171031 [St] Status: MEDLINE [do] DOI: 10.1111/sji.12576

7 / 8510

MEDLINE

seleciona para imprimir Fotocópia

[PMID]: 28982883 [Au] Autor: Hayano A; Komohara Y; Takashima Y; Takeya H; Homma J; Fukai J; Iwadate Y; Kajiwara K; Ishizawa S; Hondoh H; Yamanaka R [Ad] Endereço: Laboratory of Molecular Target Therapy for Cancer, Graduate School for Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. [Ti] Título: Programmed Cell Death Ligand 1 Expression in Primary Central Nervous System Lymphomas: A Clinicopathological Study. [So] Source: Anticancer Res;37(10):5655-5666, 2017 10. [Is] ISSN: 1791-7530 [Cp] País de publicação: Greece [La] Idioma: eng [Ab] Resumo: BACKGROUND/AIM: Programmed cell death ligand 1 (PD-L1)/programmed cell death 1 (PD-1) have been shown to predict response to PD-L1/PD-1-targeted therapy. We analyzed PD-L1 expression in primary central nervous system lymphomas (PCNSLs). MATERIALS AND METHODS: PD-L1 protein and mRNA expression were evaluated in 64 PCNSL tissue samples. IFN-γ, IL-10, CD4, and CD8 mRNA expression was also evaluated. RESULTS: PD-L1 protein was detected in tumor cells in 2 (4.1%) cases and in tumor microenvironments in 25 (52%) cases. PD-L1 mRNA positively correlated with IFN-γ (p=0.0024) and CD4 (p=0.0005) mRNA expression. IFN-γ mRNA positively correlated with CD8 mRNA expression (p=0.0001). Furthermore, tumor cell PD-L1 expression correlated positively with overall survival (p=0.0177), whereas microenvironmental PD-L1 expression exhibited an insignificant negative trend with overall survival (p=0.188). CONCLUSION: PD-L1 was expressed on both tumor and/or tumor-infiltrating immune cells in PCNSL. The biological roles of this marker warrant further investigation. [Mh] Termos MeSH primário: Antígeno B7-H1 Biomarcadores Tumorais Neoplasias do Sistema Nervoso Central/química Neoplasias do Sistema Nervoso Central/genética Linfoma/química Linfoma/genética [Mh] Termos MeSH secundário: Adulto Idoso Idoso de 80 Anos ou mais Antígeno B7-H1/análise Antígeno B7-H1/genética Biomarcadores Tumorais/análise Biomarcadores Tumorais/genética Antígenos CD4/genética Linfócitos T CD4-Positivos/química Linfócitos T CD4-Positivos/patologia Antígenos CD8/genética Linfócitos T CD8-Positivos/química Linfócitos T CD8-Positivos/patologia Neoplasias do Sistema Nervoso Central/mortalidade Neoplasias do Sistema Nervoso Central/patologia Intervalo Livre de Doença Feminino Seres Humanos Interferon gama/genética Interleucina-10/genética Estimativa de Kaplan-Meier Linfócitos do Interstício Tumoral/química Linfócitos do Interstício Tumoral/patologia Linfoma/mortalidade Linfoma/patologia Masculino Meia-Idade Modelos de Riscos Proporcionais RNA Mensageiro/genética Estudos Retrospectivos Microambiente Tumoral [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (B7-H1 Antigen); 0 (Biomarkers, Tumor); 0 (CD274 protein, human); 0 (CD4 Antigens); 0 (CD8 Antigens); 0 (IFNG protein, human); 0 (IL10 protein, human); 0 (RNA, Messenger); 130068-27-8 (Interleukin-10); 82115-62-6 (Interferon-gamma) [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: 171007 [St] Status: MEDLINE

8 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 28977602 [Au] Autor: Brown SM; Smith CE; Meuth AI; Khan M; Aroor AR; Cleeton HM; Meininger GA; Sowers JR; DeMarco VG; Chandrasekar B; Nistala R; Bender SB [Ad] Endereço: Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri 65201. [Ti] Título: Dipeptidyl Peptidase-4 Inhibition With Saxagliptin Ameliorates Angiotensin II-Induced Cardiac Diastolic Dysfunction in Male Mice. [So] Source: Endocrinology;158(10):3592-3604, 2017 Oct 01. [Is] ISSN: 1945-7170 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Activation of the renin-angiotensin-aldosterone system is common in hypertension and obesity and contributes to cardiac diastolic dysfunction, a condition for which no treatment currently exists. In light of recent reports that antihyperglycemia incretin enhancing dipeptidyl peptidase (DPP)-4 inhibitors exert cardioprotective effects, we examined the hypothesis that DPP-4 inhibition with saxagliptin (Saxa) attenuates angiotensin II (Ang II)-induced cardiac diastolic dysfunction. Male C57BL/6J mice were infused with either Ang II (500 ng/kg/min) or vehicle for 3 weeks receiving either Saxa (10 mg/kg/d) or placebo during the final 2 weeks. Echocardiography revealed Ang II-induced diastolic dysfunction, evidenced by impaired septal wall motion and prolonged isovolumic relaxation, coincident with aortic stiffening. Ang II induced cardiac hypertrophy, coronary periarterial fibrosis, TRAF3-interacting protein 2 (TRAF3IP2)-dependent proinflammatory signaling [p-p65, p-c-Jun, interleukin (IL)-17, IL-18] associated with increased cardiac macrophage, but not T cell, gene expression. Flow cytometry revealed Ang II-induced increases of cardiac CD45+F4/80+CD11b+ and CD45+F4/80+CD11c+ macrophages and CD45+CD4+ lymphocytes. Treatment with Saxa reduced plasma DPP-4 activity and abrogated Ang II-induced cardiac diastolic dysfunction independent of aortic stiffening or blood pressure. Furthermore, Saxa attenuated Ang II-induced periarterial fibrosis and cardiac inflammation, but not hypertrophy or cardiac macrophage infiltration. Analysis of Saxa-induced changes in cardiac leukocytes revealed Saxa-dependent reduction of the Ang II-mediated increase of cardiac CD11c messenger RNA and increased cardiac CD8 gene expression and memory CD45+CD8+CD44+ lymphocytes. In summary, these results demonstrate that DPP-4 inhibition with Saxa prevents Ang II-induced cardiac diastolic dysfunction, fibrosis, and inflammation associated with unique shifts in CD11c-expressing leukocytes and CD8+ lymphocytes. [Mh] Termos MeSH primário: Adamantano/análogos & derivados Aorta/efeitos dos fármacos Diástole/efeitos dos fármacos Dipeptídeos/farmacologia Inibidores da Dipeptidil Peptidase IV/farmacologia Coração/efeitos dos fármacos Rigidez Vascular/efeitos dos fármacos [Mh] Termos MeSH secundário: Adamantano/farmacologia Proteínas Adaptadoras de Transdução de Sinal/efeitos dos fármacos Proteínas Adaptadoras de Transdução de Sinal/metabolismo Angiotensina II/toxicidade Animais Pressão Sanguínea/efeitos dos fármacos Linfócitos T CD4-Positivos/efeitos dos fármacos Antígenos CD8/efeitos dos fármacos Antígenos CD8/metabolismo Cardiomegalia/induzido quimicamente Dipeptidil Peptidase 4/efeitos dos fármacos Dipeptidil Peptidase 4/metabolismo Ecocardiografia Fibrose/induzido quimicamente Expressão Gênica/efeitos dos fármacos Coração/fisiopatologia Inflamação Interleucina-17/metabolismo Interleucina-18/metabolismo Linfócitos/efeitos dos fármacos Macrófagos/efeitos dos fármacos Macrófagos/metabolismo Masculino Camundongos Proteínas Proto-Oncogênicas c-jun/efeitos dos fármacos Proteínas Proto-Oncogênicas c-jun/metabolismo Transdução de Sinais Vasoconstritores/toxicidade [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Adaptor Proteins, Signal Transducing); 0 (CD8 Antigens); 0 (Dipeptides); 0 (Dipeptidyl-Peptidase IV Inhibitors); 0 (Interleukin-17); 0 (Interleukin-18); 0 (Proto-Oncogene Proteins c-jun); 0 (Traf3ip2 protein, mouse); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); 9GB927LAJW (saxagliptin); EC 3.4.14.5 (Dipeptidyl Peptidase 4); PJY633525U (Adamantane) [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: 171005 [St] Status: MEDLINE [do] DOI: 10.1210/en.2017-00416

9 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[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

10 / 8510

MEDLINE

seleciona para imprimir Fotocópia Texto completo

[PMID]: 28771609 [Au] Autor: Gil-Pulido J; Cochain C; Lippert MA; Schneider N; Butt E; Amézaga N; Zernecke A [Ad] Endereço: Institute of Experimental Biomedicine, University Hospital Würzburg, Würzburg, Germany. [Ti] Título: Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice. [So] Source: PLoS One;12(8):e0181947, 2017. [Is] ISSN: 1932-6203 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Atherosclerosis is the main underlying cause for cardiovascular events such as myocardial infarction and stroke and its development might be influenced by immune cells. Dendritic cells (DCs) bridge innate and adaptive immune responses by presenting antigens to T cells and releasing a variety of cytokines. Several subsets of DCs can be discriminated that engage specific transcriptional pathways for their development. Basic leucine zipper transcription factor ATF-like 3 (Batf3) is required for the development of classical CD8α+ and CD103+ DCs. By crossing mice deficient in Batf3 with atherosclerosis-prone low density lipoprotein receptor (Ldlr-/-)-deficient mice we here aimed to further address the contribution of Batf3-dependent CD8α+ and CD103+ antigen-presenting cells to atherosclerosis. We demonstrate that deficiency in Batf3 entailed mild effects on the immune response in the spleen but did not alter atherosclerotic lesion formation in the aorta or aortic root, nor affected plaque phenotype in low density lipoprotein receptor-deficient mice fed a high fat diet. We thus provide evidence that Batf3-dependent antigen-presenting cells do not have a prominent role in atherosclerosis. [Mh] Termos MeSH primário: Apresentação do Antígeno/imunologia Fatores de Transcrição de Zíper de Leucina Básica/fisiologia Placa Aterosclerótica/patologia Receptores de LDL/fisiologia Proteínas Repressoras/fisiologia Linfócitos T/imunologia [Mh] Termos MeSH secundário: Animais Antígenos CD8/metabolismo Células Cultivadas Células Dendríticas/imunologia Feminino Masculino Camundongos Camundongos Endogâmicos C57BL Camundongos Knockout Placa Aterosclerótica/genética Placa Aterosclerótica/imunologia Baço/imunologia Baço/metabolismo Baço/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Basic-Leucine Zipper Transcription Factors); 0 (CD8 Antigens); 0 (Receptors, LDL); 0 (Repressor Proteins); 0 (SNFT protein, mouse) [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: 170804 [St] Status: MEDLINE [do] DOI: 10.1371/journal.pone.0181947

---

página 1 de 851

ir para página

Refinar a pesquisa

Base de dados : MEDLINE

Formulário avançado

		Pesquisar	no campo
1			PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2
2	and or and not		PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2
3	and or and not		PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2

Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde