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  1 / 1091 MEDLINE  
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[PMID]:29182664
[Au] Autor:Thanapati S; Ganu MA; Tripathy AS
[Ad] Endereço:Hepatitis Group, National Institute of Virology, Pune, Pashan, Pune, Maharashtra, India.
[Ti] Título:Differential inhibitory and activating NK cell receptor levels and NK/NKT-like cell functionality in chronic and recovered stages of chikungunya.
[So] Source:PLoS One;12(11):e0188342, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The role of natural killer (NK; CD3-CD56+)/NKT (CD3+CD56+)-like cells in chikungunya virus (CHIKV) disease progression/recovery remains unclear. Here, we investigated the expression profiles and function of NK and NKT-like cells from 35 chronic chikungunya patients, 30 recovered individuals, and 69 controls. Percentage of NKT-like cells was low in chronic chikungunya patients. NKp30+, CD244+, DNAM-1+, and NKG2D+ NK cell percentages were also lower (MFI and/or percentage), while those of CD94+ and NKG2A+ NKT-like cells were higher (MFI and/or percentage) in chronic patients than in recovered subjects. IFN-γ and TNF-α expression on NKT-like cells was high in the chronic patients, while only IFN-γ expression on NK cells was high in the recovered individuals. Furthermore, percentage of perforin+NK cells was low in the chronic patients. Lower cytotoxic activity was observed in the chronic patients than in the controls. CD107a expression on NK and NKT-like cells post anti-CD94/anti-NKG2A blocking was comparable among the patients and controls. Upregulated inhibitory and downregulated activating NK receptor expressions on NK/NKT-like cells, lower perforin+ and CD107a+NK cells are likely responsible for inhibiting the NK and NKT-like cell function in the chronic stage of chikungunya. Therefore, deregulation of NKR expression might underlie CHIKV-induced chronicity.
[Mh] Termos MeSH primário: Febre de Chikungunya/imunologia
Células Matadoras Naturais/imunologia
Células T Matadoras Naturais/imunologia
Receptores de Células Matadoras Naturais/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Criança
Feminino
Seres Humanos
Interferon gama/metabolismo
Células Matadoras Naturais/metabolismo
Masculino
Meia-Idade
Células T Matadoras Naturais/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Natural Killer Cell); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[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:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188342


  2 / 1091 MEDLINE  
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[PMID]:28835459
[Au] Autor:Netter P; Anft M; Watzl C
[Ad] Endereço:Department of Immunology, IfADo-Leibniz Research Centre for Working Environment and Human Factors, Technical University Dortmund, 44139 Dortmund, Germany; and.
[Ti] Título:Termination of the Activating NK Cell Immunological Synapse Is an Active and Regulated Process.
[So] Source:J Immunol;199(7):2528-2535, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cellular cytotoxicity is essential for the elimination of virus-infected and cancerous cells by NK cells. It requires a direct cellular contact through the establishment of an immunological synapse (IS) between the NK cell and the target cell. In this article, we show that not only the establishment of the IS, but also its maintenance is a highly regulated process. Ongoing receptor-proximal signaling events from activating NK cell receptors and actin dynamics were necessary to maintain a stable contact in an energy-dependent fashion, even after the IS was formed successfully. More importantly, the initiation of a contact to a new susceptible target cell resulted in accelerated detachment from an old target cell. We propose that the maintenance of an existing IS is a dynamic and regulated process to allow for effective serial killing of NK cells.
[Mh] Termos MeSH primário: Sinapses Imunológicas
Células Matadoras Naturais/imunologia
Ativação Linfocitária/fisiologia
[Mh] Termos MeSH secundário: Células Cultivadas
Citotoxicidade Imunológica
Células HeLa
Seres Humanos
Células K562
Receptores de Células Matadoras Naturais/genética
Receptores de Células Matadoras Naturais/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Natural Killer Cell)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700394


  3 / 1091 MEDLINE  
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[PMID]:28767726
[Au] Autor:Mahapatra S; Mace EM; Minard CG; Forbes LR; Vargas-Hernandez A; Duryea TK; Makedonas G; Banerjee PP; Shearer WT; Orange JS
[Ad] Endereço:Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas, United States of America.
[Ti] Título:High-resolution phenotyping identifies NK cell subsets that distinguish healthy children from adults.
[So] Source:PLoS One;12(8):e0181134, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are critical in immune defense against infected, stressed or transformed cells. Their function is regulated by the heterogeneous expression of a wide array of surface receptors that shape its phenotypic diversity. Although NK cells develop in the bone marrow and secondary lymphoid tissues, substantive differentiation is apparent in the peripheral blood including known age-related variation. In order to gain greater insight into phenotypic and functional variation within peripheral blood NK cells across age groups, we used multi-parametric, polyfunctional flow cytometry to interrogate the NK cell variability in 20 healthy adults and 15 5-10, 11-15 and 16-20 year-old children. We found that the normative ranges in both adults and children displayed great inter-individual variation for most markers. While the expression of several receptors did not differ, among those that did, the majority of the differences existed between adults and the three pediatric groups, rather than among children of different ages. Interestingly, we also identified variation in the individual expression of some markers by sex and ethnicity. Combinatorial analysis of NK cell receptors revealed intermediate subsets between the CD56bright and CD56dim NK cells. Furthermore, on examining the NK cell diversity by age, adults were discovered to have the lowest developmental diversity. Thus, our findings identify previously unappreciated NK cell subsets potentially distinguishing children from adults and suggest functional correlates that may have relevance in age-specific host defense.
[Mh] Termos MeSH primário: Imunofenotipagem
Células Matadoras Naturais/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Fatores Etários
Antígeno CD56/metabolismo
Criança
Análise por Conglomerados
Feminino
Citometria de Fluxo
Seres Humanos
Células Matadoras Naturais/citologia
Células Matadoras Naturais/imunologia
Leucócitos Mononucleares/citologia
Meia-Idade
Receptores de Células Matadoras Naturais/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD56 Antigen); 0 (Receptors, Natural Killer Cell)
[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:170803
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181134


  4 / 1091 MEDLINE  
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[PMID]:28695291
[Au] Autor:Hilton HG; Parham P
[Ad] Endereço:Departments of Structural Biology and Microbiology & Immunology, Stanford University, Fairchild D-159, 299 Campus Drive West, Stanford, CA, 94305, USA.
[Ti] Título:Missing or altered self: human NK cell receptors that recognize HLA-C.
[So] Source:Immunogenetics;69(8-9):567-579, 2017 Aug.
[Is] ISSN:1432-1211
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are fast-acting and versatile lymphocytes that are critical effectors of innate immunity, adaptive immunity, and placental development. Controlling NK cell function are the interactions between killer-cell immunoglobulin-like receptors (KIRs) and their HLA-A, HLA-B and HLA-C ligands. Due to the extensive polymorphism of both KIR and HLA class I, these interactions are highly diversified and specific combinations correlate with protection or susceptibility to a range of infectious, autoimmune, and reproductive disorders. Evolutionary, genetic, and functional studies are consistent with the interactions between KIR and HLA-C being the dominant control mechanism of human NK cells. In addition to their recognition of the C1 and C2 epitopes, increasing evidence points to KIR having a previously unrecognized selectivity for the peptide presented by HLA-C. This selectivity appears to be a conserved feature of activating KIR and may partly explain the slow progress made in identifying their HLA class I ligands. The peptide selectivity of KIR allows NK cells to respond, not only to changes in the surface expression of HLA-C, but also to the more subtle changes in the HLA-C peptidome, such as occur during viral infection and malignant transformation. Here, we review recent advances in understanding of human-specific KIR evolution and how the inhibitory and activating HLA-C receptors allow NK cells to respond to healthy cells, diseased cells, and the semi-allogeneic cells of the fetus.
[Mh] Termos MeSH primário: Antígenos HLA-C/fisiologia
Receptores de Células Matadoras Naturais/fisiologia
[Mh] Termos MeSH secundário: Haplótipos
Seres Humanos
Receptores KIR/fisiologia
Receptores KIR2DL1/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HLA-C Antigens); 0 (Receptors, KIR); 0 (Receptors, KIR2DL1); 0 (Receptors, Natural Killer Cell)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1007/s00251-017-1001-y


  5 / 1091 MEDLINE  
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[PMID]:28636952
[Au] Autor:Dulberger CL; McMurtrey CP; Hölzemer A; Neu KE; Liu V; Steinbach AM; Garcia-Beltran WF; Sulak M; Jabri B; Lynch VJ; Altfeld M; Hildebrand WH; Adams EJ
[Ad] Endereço:Department of Biochemistry and Molecular Biology, The University of Chicago, Chicago, IL 60637, USA.
[Ti] Título:Human Leukocyte Antigen F Presents Peptides and Regulates Immunity through Interactions with NK Cell Receptors.
[So] Source:Immunity;46(6):1018-1029.e7, 2017 Jun 20.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Evidence is mounting that the major histocompatibility complex (MHC) molecule HLA-F (human leukocyte antigen F) regulates the immune system in pregnancy, infection, and autoimmunity by signaling through NK cell receptors (NKRs). We present structural, biochemical, and evolutionary analyses demonstrating that HLA-F presents peptides of unconventional length dictated by a newly arisen mutation (R62W) that has produced an open-ended groove accommodating particularly long peptides. Compared to empty HLA-F open conformers (OCs), HLA-F tetramers bound with human-derived peptides differentially stained leukocytes, suggesting peptide-dependent engagement. Our in vitro studies confirm that NKRs differentiate between peptide-bound and peptide-free HLA-F. The complex structure of peptide-loaded ß m-HLA-F bound to the inhibitory LIR1 revealed similarities to high-affinity recognition of the viral MHC-I mimic UL18 and a docking strategy that relies on contacts with HLA-F as well as ß m, thus precluding binding to HLA-F OCs. These findings provide a biochemical framework to understand how HLA-F could regulate immunity via interactions with NKRs.
[Mh] Termos MeSH primário: Antígenos de Histocompatibilidade Classe I/metabolismo
Células Matadoras Naturais/imunologia
Mimetismo Molecular
Receptores de Células Matadoras Naturais/metabolismo
Proteínas Virais/química
[Mh] Termos MeSH secundário: Apresentação do Antígeno
Antígenos/imunologia
Antígenos/metabolismo
Antígenos CD/metabolismo
Evolução Biológica
Cristalografia por Raios X
Feminino
Células HEK293
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Mutação/genética
Fragmentos de Peptídeos/imunologia
Fragmentos de Peptídeos/metabolismo
Gravidez
Ligação Proteica
Conformação Proteica
Receptores Imunológicos/metabolismo
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Antigens, CD); 0 (HLA-F antigens); 0 (Histocompatibility Antigens Class I); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Peptide Fragments); 0 (Receptors, Immunologic); 0 (Receptors, Natural Killer Cell); 0 (Viral Proteins)
[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:170622
[St] Status:MEDLINE


  6 / 1091 MEDLINE  
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[PMID]:28586095
[Au] Autor:Makwana N; Foley B; Fernandez S; Lee S; Irish A; Pircher H; Price P
[Ad] Endereço:Pathology & Laboratory Medicine, University of Western Australia, Nedlands, Australia.
[Ti] Título:CMV drives the expansion of highly functional memory T cells expressing NK-cell receptors in renal transplant recipients.
[So] Source:Eur J Immunol;47(8):1324-1334, 2017 Aug.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Cytomegalovirus (CMV) is a common opportunistic infection encountered in renal transplant recipients (RTRs) and may be reactivated without symptoms at any time post-transplant. We describe how active and latent CMV affect T-cell subsets in RTRs who are stable on maintenance therapy. T-cell responses to CMV were assessed in RTRs (n = 54) >2 years post-transplant, and healthy controls (n = 38). Seven RTRs had CMV DNA detectable in plasma. CMV antibody and DNA aligned with increased proportions of CD8 T cells and reduced CD4/CD8 ratios. This paralleled an expansion of effector memory T-cell (T ), terminally differentiated T-cell (T ) and CD57 T cell populations. Expression of NK-cell receptors, LIR-1 and KLRG1 on CD4 and CD8 CD57 T and T cells correlated with elevated interferon-γ and cytotoxic responses to anti-CD3 and increased cytotoxic responses to CMV phosphoprotein (pp) 65 in RTRs who carried CMV DNA. CD8 T cells from all CMV seropositive RTRs responded efficiently to CMV immediate early (IE) -1 peptides. The data show that latent and active CMV infection can alter T-cell subsets in RTRs many years after transplantation, and up-regulate T-cell expression of NK-cell receptors. This may enhance effector responses of CD4 and CD8 T cells against CMV.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Memória Imunológica
Transplante de Rim
Lectinas Tipo C/metabolismo
Receptores Imunológicos/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígenos CD/genética
Relação CD4-CD8
Antígenos CD57/genética
Antígenos CD57/imunologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/imunologia
Citomegalovirus/genética
Infecções por Citomegalovirus/virologia
DNA Viral/sangue
Feminino
Genes Precoces
Seres Humanos
Interferon gama/biossíntese
Interferon gama/imunologia
Células Matadoras Naturais/imunologia
Lectinas Tipo C/genética
Receptor B1 de Leucócitos Semelhante a Imunoglobulina
Masculino
Meia-Idade
Peptídeos/farmacologia
Receptores Imunológicos/genética
Receptores de Células Matadoras Naturais/genética
Receptores de Células Matadoras Naturais/metabolismo
Transativadores/genética
Transplantados
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD57 Antigens); 0 (DNA, Viral); 0 (KLRG1 protein, human); 0 (LILRB1 protein, human); 0 (Lectins, C-Type); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (Peptides); 0 (Receptors, Immunologic); 0 (Receptors, Natural Killer Cell); 0 (Trans-Activators); 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:170607
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747018


  7 / 1091 MEDLINE  
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[PMID]:28494934
[Au] Autor:Altmeyer S; Zentek J; Vahjen W; Scharek-Tedin L
[Ad] Endereço:Institute of Animal Nutrition, Department of Veterinary Medicine, Freie Universität Berlin, Königin-Luise-Strasse 49, D-14195 Berlin, Germany. Electronic address: Sara.Altmeyer@fu-berlin.de.
[Ti] Título:The expression of NKG2D on porcine IEL and its possible relation to the adaptive intestinal immune system.
[So] Source:Vet Immunol Immunopathol;187:89-95, 2017 May.
[Is] ISSN:1873-2534
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The gastrointestinal tract contains a multitude of components which include intraepithelial lymphocytes (IEL). IELs have been reported to express a variety of surface receptors that enable cross talk among various cell populations. The purpose of the reported investigation was to determine which IEL populations express the natural killer cell receptor NKG2D which is an activating receptor that plays a role in cytolytic responses. In a feeding experiment with piglets, IELs were isolated from jejunal tissue at three different stages post weaning. The time dependent development of different cell populations was evaluated and an elevated number of lymphocytes (CD45+) shortly after weaning was observed compared to later time points. The number of T cells (CD3), including cytotoxic T cells (CD8ß/CD16-), appeared to be particularly affected by the weaning period. Correlation analysis revealed an association between the NKG2D expression in jejunal tissue and the frequency of lymphocytes, esp. CD8ß+ cytotoxic T cells. Gene expression analysis of NKG2D were performed on several isolated IEL populations and support the hypothesis that cytotoxic T cells (CD8ß) in the porcine gut epithelium are capable of communicating with the surrounding enterocytes and inducing immune reactions via NKG2D. Unlike previous observations in porcine blood, the γδ T cells of the gut epithelium also showed expression of the stress factor binding NKG2D receptor. Subsequent analysis of the isolated IELs revealed that T cells appear to only express the receptor after isolation with an anti-CD3 mab, indicating that a previous stimulation of the TCR/CD3 complex may reinforce this signal transduction pathway.
[Mh] Termos MeSH primário: Intestinos/imunologia
Receptores de Células Matadoras Naturais/fisiologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Animais
Feminino
Citometria de Fluxo/veterinária
Mucosa Intestinal/citologia
Mucosa Intestinal/imunologia
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/fisiologia
Masculino
Receptores de Células Matadoras Naturais/imunologia
Suínos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Natural Killer Cell)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE


  8 / 1091 MEDLINE  
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[PMID]:28386908
[Au] Autor:Meazza R; Falco M; Marcenaro S; Loiacono F; Canevali P; Bellora F; Tuberosa C; Locatelli F; Micalizzi C; Moretta A; Mingari MC; Moretta L; Aricò M; Bottino C; Pende D
[Ad] Endereço:Dipartimento delle Terapie Oncologiche Integrate, IRCCS AOU San Martino-IST, Genoa, Italy.
[Ti] Título:Inhibitory 2B4 contributes to NK cell education and immunological derangements in XLP1 patients.
[So] Source:Eur J Immunol;47(6):1051-1061, 2017 Jun.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:X-linked lymphoproliferative disease 1 (XLP1) is an inherited immunodeficiency, caused by mutations in SH2D1A encoding Signaling Lymphocyte Activation Molecule (SLAM)-associated protein (SAP). In XLP1, 2B4, upon engagement with CD48, has inhibitory instead of activating function. This causes a selective inability of cytotoxic effectors to kill EBV-infected cells, with dramatic clinical sequelae. Here, we investigated the NK cell education in XLP1, upon characterization of killer Ig-like receptor (KIR)/KIR-L genotype and phenotypic repertoire of self-HLA class I specific inhibitory NK receptors (self-iNKRs). We also analyzed NK-cell cytotoxicity against CD48 or CD48 KIR-ligand matched or autologous hematopoietic cells in XLP1 patients and healthy controls. XLP1 NK cells may show a defective phenotypic repertoire with substantial proportion of cells lacking self-iNKR. These NK cells are cytotoxic and the inhibitory 2B4/CD48 pathway plays a major role to prevent killing of CD48 EBV-transformed B cells and M1 macrophages. Importantly, self-iNKR defective NK cells kill CD48 targets, such as mature DCs. Self-iNKR NK cells in XLP1 patients are functional even in resting conditions, suggesting a role of the inhibitory 2B4/CD48 pathway in the education process during NK-cell maturation. Killing of autologous mature DC by self-iNKR defective XLP1 NK cells may impair adaptive responses, further exacerbating the patients' immune defect.
[Mh] Termos MeSH primário: Células Matadoras Naturais/imunologia
Transtornos Linfoproliferativos/imunologia
Transtornos Linfoproliferativos/fisiopatologia
Receptores de Células Matadoras Naturais/imunologia
Família de Moléculas de Sinalização da Ativação Linfocitária/metabolismo
[Mh] Termos MeSH secundário: Antígeno CD48/imunologia
Antígeno CD48/metabolismo
Genes MHC Classe I
Seres Humanos
Células Matadoras Naturais/metabolismo
Ativação Linfocitária
Canais de Potássio Corretores do Fluxo de Internalização/imunologia
Receptores Imunológicos/metabolismo
Transdução de Sinais
Proteína Associada à Molécula de Sinalização da Ativação Linfocitária/metabolismo
Família de Moléculas de Sinalização da Ativação Linfocitária/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD244 protein, human); 0 (CD48 Antigen); 0 (CD48 protein, human); 0 (Kcnj10 (channel)); 0 (Potassium Channels, Inwardly Rectifying); 0 (Receptors, Immunologic); 0 (Receptors, Natural Killer Cell); 0 (Signaling Lymphocytic Activation Molecule Associated Protein); 0 (Signaling Lymphocytic Activation Molecule Family)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646885


  9 / 1091 MEDLINE  
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[PMID]:28346697
[Au] Autor:DeSelm CJ; Tano ZE; Varghese AM; Adusumilli PS
[Ad] Endereço:Center for Cell Engineering, Memorial Sloan Kettering Cancer Center, New York, New York.
[Ti] Título:CAR T-cell therapy for pancreatic cancer.
[So] Source:J Surg Oncol;116(1):63-74, 2017 Jul.
[Is] ISSN:1096-9098
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chimeric antigen receptor (CAR) T-cell therapy utilizes genetic engineering to redirect a patient's own T cells to target cancer cells. The remarkable results in hematological malignancies prompted investigating this approach in solid tumors such as pancreatic cancer. The complex tumor microenvironment, stromal hindrance in limiting immune response, and expression of checkpoint blockade on T cells pose hurdles. Herein, we summarize the opportunities, challenges, and state of knowledge in targeting pancreatic cancer with CAR T-cell therapy.
[Mh] Termos MeSH primário: Imunoterapia Adotiva
Neoplasias Pancreáticas/imunologia
Neoplasias Pancreáticas/terapia
Linfócitos T/transplante
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/imunologia
Antígeno CD24/imunologia
Antígeno Carcinoembrionário/imunologia
Ensaios Clínicos como Assunto
Proteínas Ligadas por GPI/imunologia
Seres Humanos
Mucina-1/imunologia
Proteínas de Neoplasias/imunologia
Receptor ErbB-2/imunologia
Receptores de Antígenos de Linfócitos T
Receptores de Células Matadoras Naturais/imunologia
Células Estromais/imunologia
Linfócitos T/imunologia
Condicionamento Pré-Transplante
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (CD24 Antigen); 0 (CD24 protein, human); 0 (Carcinoembryonic Antigen); 0 (GPI-Linked Proteins); 0 (MUC1 protein, human); 0 (Mucin-1); 0 (Neoplasm Proteins); 0 (PSCA protein, human); 0 (Receptors, Antigen, T-Cell); 0 (Receptors, Natural Killer Cell); 0 (mesothelin); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[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:170328
[St] Status:MEDLINE
[do] DOI:10.1002/jso.24627


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[PMID]:28340350
[Au] Autor:Aguilar OA; Berry R; Rahim MM; Reichel JJ; Popovic B; Tanaka M; Fu Z; Balaji GR; Lau TN; Tu MM; Kirkham CL; Mahmoud AB; Mesci A; Krmpotic A; Allan DS; Makrigiannis AP; Jonjic S; Rossjohn J; Carlyle JR
[Ad] Endereço:Department of Immunology, University of Toronto, Toronto, ON M5S 1A8, Canada; Sunnybrook Research Institute, Toronto, ON M4N 3M5, Canada.
[Ti] Título:A Viral Immunoevasin Controls Innate Immunity by Targeting the Prototypical Natural Killer Cell Receptor Family.
[So] Source:Cell;169(1):58-71.e14, 2017 Mar 23.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells play a key role in innate immunity by detecting alterations in self and non-self ligands via paired NK cell receptors (NKRs). Despite identification of numerous NKR-ligand interactions, physiological ligands for the prototypical NK1.1 orphan receptor remain elusive. Here, we identify a viral ligand for the inhibitory and activating NKR-P1 (NK1.1) receptors. This murine cytomegalovirus (MCMV)-encoded protein, m12, restrains NK cell effector function by directly engaging the inhibitory NKR-P1B receptor. However, m12 also interacts with the activating NKR-P1A/C receptors to counterbalance m12 decoy function. Structural analyses reveal that m12 sequesters a large NKR-P1 surface area via a "polar claw" mechanism. Polymorphisms in, and ablation of, the viral m12 protein and host NKR-P1B/C alleles impact NK cell responses in vivo. Thus, we identify the long-sought foreign ligand for this key immunoregulatory NKR family and reveal how it controls the evolutionary balance of immune recognition during host-pathogen interplay.
[Mh] Termos MeSH primário: Células Matadoras Naturais/imunologia
Muromegalovirus/imunologia
Receptores de Células Matadoras Naturais/imunologia
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos Ly/metabolismo
Linhagem Celular
Células HEK293
Interações Hospedeiro-Patógeno
Seres Humanos
Evasão da Resposta Imune
Imunidade Inata
Camundongos
Células NIH 3T3
Subfamília B de Receptores Semelhantes a Lectina de Células NK/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Ly); 0 (Klrb1b protein, mouse); 0 (Klrb1c protein, mouse); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Receptors, Natural Killer Cell); 0 (Viral Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE



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