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Pesquisa : A11.066.270 [Categoria DeCS]
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[PMID]:29455234
[Au] Autor:Wang S; Wang X; Liu M; Bai O
[Ad] Endereço:Department of Hematology, The First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
[Ti] Título:Blastic plasmacytoid dendritic cell neoplasm: update on therapy especially novel agents.
[So] Source:Ann Hematol;97(4):563-572, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Células Dendríticas/efeitos dos fármacos
Drogas em Investigação/uso terapêutico
Neoplasias Hematológicas/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linhagem Celular Tumoral
Neoplasias do Sistema Nervoso Central/diagnóstico
Neoplasias do Sistema Nervoso Central/prevenção & controle
Neoplasias do Sistema Nervoso Central/secundário
Células Dendríticas/patologia
Drogas em Investigação/farmacologia
Neoplasias Hematológicas/diagnóstico
Neoplasias Hematológicas/patologia
Neoplasias Hematológicas/cirurgia
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Seres Humanos
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drugs, Investigational)
[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:180219
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3259-z


  2 / 39211 MEDLINE  
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[PMID]:29381830
[Au] Autor:Sioud M
[Ad] Endereço:Department of Cancer Immunology, Oslo University Hospital, The Norwegian Radium Hospital, Montebello, Oslo, Norway.
[Ti] Título:T-cell cross-reactivity may explain the large variation in how cancer patients respond to checkpoint inhibitors.
[So] Source:Scand J Immunol;87(3), 2018 Mar.
[Is] ISSN:1365-3083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The therapeutic use of the immune system to specifically attack tumours has been a long-standing vision among tumour immunologists. Recently, the use of checkpoint inhibitors to turn-off immunosuppressive signals has proven to be effective in enhancing T-cell reactivity against patient-specific neoantigens, resulting from somatic mutations. Several of the identified T-cell epitopes share similarity with common bacterial and viral antigens, suggesting the involvement of pre-existing microbial cross-reactive T cells in rapid and durable tumour regression seen in some patients. This notion of T-cell cross-reactivity is further supported by the findings that intestinal bacteria can influence checkpoint-blockade therapy. Moreover, early data indicate the presence of such T cells in long-term survival breast cancer patients. This review highlights the main challenges for cancer immunotherapy and discusses the potential contribution of T-cell cross-reactivity in cancer immunotherapy and whether it can be used as a biomarker to predict the responsiveness to checkpoint inhibitors.
[Mh] Termos MeSH primário: Reações Cruzadas/imunologia
Imunoterapia/métodos
Neoplasias/imunologia
Neoplasias/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígenos de Bactérias/imunologia
Antígenos de Neoplasias/imunologia
Antígenos Virais/imunologia
Biomarcadores Tumorais/imunologia
Antígeno CTLA-4/antagonistas & inibidores
Células Dendríticas/imunologia
Epitopos de Linfócito T/imunologia
Seres Humanos
Ativação Linfocitária/imunologia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptores Imunológicos/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Antigens, Neoplasm); 0 (Antigens, Viral); 0 (Biomarkers, Tumor); 0 (CTLA-4 Antigen); 0 (Epitopes, T-Lymphocyte); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (TIGIT protein, human)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1111/sji.12643


  3 / 39211 MEDLINE  
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[PMID]:29339155
[Au] Autor:Kuwabara J; Umakoshi A; Abe N; Sumida Y; Ohsumi S; Usa E; Taguchi K; Choudhury ME; Yano H; Matsumoto S; Kunieda T; Takahashi H; Yorozuya T; Watanabe Y; Tanaka J
[Ad] Endereço:Department of Gastrointestinal Surgery and Surgical Oncology, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
[Ti] Título:Truncated CD200 stimulates tumor immunity leading to fewer lung metastases in a novel Wistar rat metastasis model.
[So] Source:Biochem Biophys Res Commun;496(2):542-548, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD200 mediates immunosuppression in immune cells that express its receptor, CD200R. There are two CD200 variants; truncated CD200 that lacks the part of N-terminal sequence necessary for CD200R binding (CD200S) and full-length CD200 (CD200L). We established a novel lung metastasis model by subcutaneously transplanting C6 glioma cells into the backs of neonatal Wistar rats. All transplanted rats developed large back tumors, nearly 90% of which bore lung metastases. To compare the effects of CD200S and CD200L on tumor immunity, CD200L (C6-L)- or CD200S (C6-S)-expressing C6 cells were similarly transplanted. The results showed that 100% of rats with C6-L tumors developed lung metastases, while metastases were found in only 44% of rats with C6-S tumors (n = 25). Tumors disappeared in approximately 20% of the C6-S-bearing rats, and these animals evaded death 180 d after transplantation, while all C6-L tumor-bearing rats died after 45 d. Next generation sequencing revealed that C6-S tumors expressed chemokines and granzyme B at much higher levels than C6-L tumors. Flow cytometry revealed that C6-S tumors contained more dead cells and more CD45 cells, including natural killer cells and CD8 lymphocytes. In particular, multiple subsets of dendritic cells expressing CD11c, MHC class II, CD8, and/or CD103 were more abundant in C6-S than in C6-L tumors. These results suggested that CD200S induced the accumulation of multiple dendritic cell subsets that activated cytotoxic T lymphocytes, leading to the elimination of metastasizing tumor cells.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
Glioma/imunologia
Glioma/patologia
Neoplasias Pulmonares/imunologia
Neoplasias Pulmonares/secundário
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Células Dendríticas/imunologia
Células Dendríticas/patologia
Regulação Neoplásica da Expressão Gênica
Glioma/genética
Tolerância Imunológica
Imunidade Celular
Pulmão/imunologia
Pulmão/patologia
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/patologia
Mutação
Ratos Wistar
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (antigens, CD200)
[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:180118
[St] Status:MEDLINE


  4 / 39211 MEDLINE  
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[PMID]:29180487
[Au] Autor:Pierog PL; Zhao Y; Singh S; Dai J; Yap GS; Fitzgerald-Bocarsly P
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103.
[Ti] Título: Inactivates Human Plasmacytoid Dendritic Cells by Functional Mimicry of IL-10.
[So] Source:J Immunol;200(1):186-195, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasmacytoid dendritic cells (pDCs) are the major producers of IFN-α, an antiviral cytokine involved in immunomodulation and control of HIV type 1 replication, whereas is a life-threatening opportunistic infection in AIDS patients. During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce lower amounts of IFN-α in response to viral stimulation. In this study, we investigated the impact of coinfection with on the innate virus-directed responses of human pDCs. Using intracellular flow cytometry and fluorescence microscopy, we determined that invaded but did not induce IFN-α or TNF-α in human pDC. However, inhibited IFN-α and TNF-α produced in response to HSV and HIV, thus functionally inactivating pDC. IFN-α production was inhibited only in cells infected by , which inhibited neither uptake of GFP-HSV nor localization of TLR9 in CD71 endosomes, directing us to investigate downstream events. Using imaging flow cytometry, we found that both and IL-10 inhibited virus-induced nuclear translocation, but not phosphorylation, of IFN response factor 7. Blockade of IFN response factor 7 nuclear translocation and inhibition of the IFN-α response was partially reversed by a deficiency in the -derived ROP16 kinase, known to directly phosphorylate STAT3, a critical mediator of IL-10's anti-inflammatory effects. Taken together, our results indicate that suppresses pDC activation by mimicking IL-10's regulatory effects through an ROP16 kinase-dependent mechanism. Our findings further imply a convergent mechanism of inhibition of TLR signaling by and IL-10 and suggest potential negative consequences of HIV/ coinfection.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Infecções por HIV/imunologia
HIV-1/imunologia
Interleucina-10/metabolismo
Infecções Oportunistas/imunologia
Proteínas Tirosina Quinases/metabolismo
Proteínas de Protozoários/metabolismo
Toxoplasma/imunologia
Toxoplasmose/imunologia
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Coinfecção
Células Dendríticas/parasitologia
Seres Humanos
Imunidade Inata
Imunomodulação
Fator Regulador 7 de Interferon/metabolismo
Interferon-alfa/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Receptor Toll-Like 9/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (IRF7 protein, human); 0 (Interferon Regulatory Factor-7); 0 (Interferon-alpha); 0 (Protozoan Proteins); 0 (STAT3 Transcription Factor); 0 (Toll-Like Receptor 9); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Rop16 protein, Toxoplasma gondii)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1701045


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[PMID]:29295985
[Au] Autor:Conrad C; Di Domizio J; Mylonas A; Belkhodja C; Demaria O; Navarini AA; Lapointe AK; French LE; Vernez M; Gilliet M
[Ad] Endereço:Department of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland. curdin.conrad@chuv.ch.
[Ti] Título:TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis.
[So] Source:Nat Commun;9(1):25, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although anti-tumor necrosis factor (TNF) agents are highly effective in the treatment of psoriasis, 2-5% of treated patients develop psoriasis-like skin lesions called paradoxical psoriasis. The pathogenesis of this side effect and its distinction from classical psoriasis remain unknown. Here we show that skin lesions from patients with paradoxical psoriasis are characterized by a selective overexpression of type I interferons, dermal accumulation of plasmacytoid dendritic cells (pDC), and reduced T-cell numbers, when compared to classical psoriasis. Anti-TNF treatment prolongs type I interferon production by pDCs through inhibition of their maturation. The resulting type I interferon overexpression is responsible for the skin phenotype of paradoxical psoriasis, which, unlike classical psoriasis, is independent of T cells. These findings indicate that paradoxical psoriasis represents an ongoing overactive innate inflammatory process, driven by pDC-derived type I interferon that does not lead to T-cell autoimmunity.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Autoimunidade/imunologia
Interferon Tipo I/imunologia
Psoríase/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Adalimumab/efeitos adversos
Adalimumab/imunologia
Adalimumab/uso terapêutico
Adolescente
Adulto
Idoso
Animais
Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Autoimunidade/efeitos dos fármacos
Células Cultivadas
Doença de Crohn/tratamento farmacológico
Doença de Crohn/imunologia
Doença de Crohn/metabolismo
Citocinas/genética
Citocinas/imunologia
Citocinas/metabolismo
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Feminino
Seres Humanos
Infliximab/efeitos adversos
Infliximab/imunologia
Infliximab/uso terapêutico
Interferon Tipo I/genética
Interferon Tipo I/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Meia-Idade
Psoríase/induzido quimicamente
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Linfócitos T/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Cytokines); 0 (Interferon Type I); 0 (Tumor Necrosis Factor-alpha); B72HH48FLU (Infliximab); FYS6T7F842 (Adalimumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02466-4


  6 / 39211 MEDLINE  
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[PMID]:28460478
[Au] Autor:Vo MC; Nguyen-Pham TN; Lee HJ; Jaya Lakshmi T; Yang S; Jung SH; Kim HJ; Lee JJ
[Ad] Endereço:Research Center for Cancer Immunotherapy, Chonnam National University Hwasun Hospital, Hwasun, Jeollanamdo, Republic of Korea.
[Ti] Título:Combination therapy with dendritic cells and lenalidomide is an effective approach to enhance antitumor immunity in a mouse colon cancer model.
[So] Source:Oncotarget;8(16):27252-27262, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we investigated efficacy of lenalidomide in combination with tumor antigen-loaded dendritic cells (DCs) in murine colon cancer model. MC-38 cell lines were injected subcutaneously to establish colon cancer-bearing mice. After tumor growth, lenalidomide (50 mg/kg/day) was injected intraperitoneally on 3 consecutive days in combination with tumor antigen-loaded DC vaccination on days 8, 12, 16, and 20. The tumor antigen-loaded DCs plus lenalidomide combination treatment exhibited a significant inhibition of tumor growth compared with the other groups. These effects were associated with a reduction in immune suppressor cells, such as myeloid-derived suppressor cells and regulatory T cells, with the induction of immune effector cells, such as natural killer cells, CD4+ T cells and CD8+ T cells in spleen, and with the activation of cytotoxic T lymphocytes and NK cells. This study suggests that a combination of tumor antigen-loaded DC vaccination and lenalidomide synergistically enhanced antitumor immune response in the murine colon cancer model, by inhibiting the generation of immune suppressive cells and recovery of effector cells, and demonstrated superior polarization of Th1/Th2 balance in favor of Th1 immune response. This combination approach with DCs and lenalidomide may provide a new therapeutic option to improve the treatment of colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/imunologia
Neoplasias do Colo/patologia
Células Dendríticas/imunologia
Imunidade
Talidomida/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Antígenos de Neoplasias/imunologia
Vacinas Anticâncer/administração & dosagem
Vacinas Anticâncer/imunologia
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Neoplasias do Colo/genética
Neoplasias do Colo/terapia
Terapia Combinada
Citocinas/biossíntese
Células Dendríticas/metabolismo
Modelos Animais de Doenças
Feminino
Expressão Gênica
Imunidade/efeitos dos fármacos
Imunoterapia
Células Matadoras Naturais/imunologia
Células Matadoras Naturais/metabolismo
Camundongos
Linfócitos T Citotóxicos/efeitos dos fármacos
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Talidomida/farmacologia
Vacinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Cancer Vaccines); 0 (Cytokines); 4Z8R6ORS6L (Thalidomide); F0P408N6V4 (lenalidomide)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15917


  7 / 39211 MEDLINE  
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[PMID]:28459443
[Au] Autor:Tavernier SJ; Osorio F; Vandersarren L; Vetters J; Vanlangenakker N; Van Isterdael G; Vergote K; De Rycke R; Parthoens E; van de Laar L; Iwawaki T; Del Valle JR; Hu CA; Lambrecht BN; Janssens S
[Ad] Endereço:Laboratory of Immunoregulation and Mucosal Immunology, VIB Center for Inflammation Research, 9052 Ghent, Belgium.
[Ti] Título:Regulated IRE1-dependent mRNA decay sets the threshold for dendritic cell survival.
[So] Source:Nat Cell Biol;19(6):698-710, 2017 Jun.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The IRE1-XBP1 signalling pathway is part of a cellular programme that protects against endoplasmic reticulum (ER) stress, but also controls development and survival of immune cells. Loss of XBP1 in splenic type 1 conventional dendritic cells (cDC1s) results in functional alterations without affecting cell survival. However, in mucosal cDC1s, loss of XBP1 impaired survival in a tissue-specific manner-while lung cDC1s die, intestinal cDC1s survive. This was not caused by differential activation of ER stress cell-death regulators CHOP or JNK. Rather, survival of intestinal cDC1s was associated with their ability to shut down protein synthesis through a protective integrated stress response and their marked increase in regulated IRE1-dependent messenger RNA decay. Furthermore, loss of IRE1 endonuclease on top of XBP1 led to cDC1 loss in the intestine. Thus, mucosal DCs differentially mount ATF4- and IRE1-dependent adaptive mechanisms to survive in the face of ER stress.
[Mh] Termos MeSH primário: Células Dendríticas/enzimologia
Mucosa Intestinal/enzimologia
Proteínas de Membrana/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Estabilidade de RNA
RNA Mensageiro/metabolismo
Mucosa Respiratória/enzimologia
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/genética
Fator 4 Ativador da Transcrição/metabolismo
Animais
Apoptose
Sobrevivência Celular
Células Dendríticas/patologia
Estresse do Retículo Endoplasmático
Genótipo
Mucosa Intestinal/patologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Proteínas de Membrana/genética
Camundongos Transgênicos
Fenótipo
Biossíntese de Proteínas
Proteínas Serina-Treonina Quinases/genética
RNA Mensageiro/genética
Mucosa Respiratória/patologia
Transdução de Sinais
Fatores de Tempo
Fator de Transcrição CHOP/genética
Fator de Transcrição CHOP/metabolismo
Resposta a Proteínas não Dobradas
Proteína 1 de Ligação a X-Box/genética
Proteína 1 de Ligação a X-Box/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atf4 protein, mouse); 0 (Ddit3 protein, mouse); 0 (Membrane Proteins); 0 (RNA, Messenger); 0 (X-Box Binding Protein 1); 0 (Xbp1 protein, mouse); 145891-90-3 (Activating Transcription Factor 4); 147336-12-7 (Transcription Factor CHOP); EC 2.7.1.- (Ern2 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3518


  8 / 39211 MEDLINE  
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[PMID]:28463086
[Au] Autor:Mann EH; Ho TR; Pfeffer PE; Matthews NC; Chevretton E; Mudway I; Kelly FJ; Hawrylowicz CM
[Ad] Endereço:1 MRC and Asthma-UK Centre for Allergic Mechanisms in Asthma, and.
[Ti] Título:Vitamin D Counteracts an IL-23-Dependent IL-17A IFN-γ Response Driven by Urban Particulate Matter.
[So] Source:Am J Respir Cell Mol Biol;57(3):355-366, 2017 09.
[Is] ISSN:1535-4989
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health. This is hypothesized to be due in part to regulation of IL-17A, which UPM is reported to promote. Here, we used a myeloid dendritic cell (DC)-memory CD4 T cell co-culture system to characterize UPM-driven IL-17A cells, investigate the mechanism by which UPM-primed DCs promote this phenotype, and address evidence for cross-regulation by vitamin D. CD1c myeloid DCs were cultured overnight with or without a reference source of UPM and/or active vitamin D (1,25[OH] D ) before they were co-cultured with autologous memory CD4 T cells. Supernatants were harvested for cytokine analysis on Day 5 of co-culture, and intracellular cytokine staining was performed on Day 7. UPM-primed DCs increased the proportion of memory CD4 T cells expressing the T helper 17 cell (Th17)-associated cytokines IL-17A, IL-17F, and IL-22, as well as IFN-γ, granulocyte-macrophage colony-stimulating factor, and granzyme B. Notably, a large proportion of the UPM-driven IL-17A cells co-expressed these cytokines, but not IL-10, indicative of a proinflammatory Th17 profile. UPM-treated DCs expressed elevated levels of il23 mRNA and increased secretion of IL-23p40. Neutralization of IL-23 in culture reduced the frequency of IL-17A IFN-γ cells without affecting cell proliferation. 1,25(OH) D counteracted the UPM-driven DC maturation and inhibited the frequency of IL-17A IFN-γ cells, most prominently when DCs were co-treated with the corticosteroid dexamethasone, while maintaining antiinflammatory IL-10 synthesis. These data indicate that UPM might promote an inflammatory milieu in part by inducing an IL-23-driven proinflammatory Th17 response. Restoring vitamin D sufficiency may counteract these UPM-driven effects without obliterating important homeostatic immune functions.
[Mh] Termos MeSH primário: Cidades
Interferon gama/metabolismo
Interleucina-17/metabolismo
Interleucina-23/metabolismo
Material Particulado/toxicidade
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Calcitriol/farmacologia
Diferenciação Celular/efeitos dos fármacos
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/metabolismo
Dexametasona/farmacologia
Seres Humanos
Células Mieloides/efeitos dos fármacos
Células Mieloides/metabolismo
Fenótipo
Células Th17/imunologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (Interleukin-17); 0 (Interleukin-23); 0 (Particulate Matter); 1406-16-2 (Vitamin D); 7S5I7G3JQL (Dexamethasone); 82115-62-6 (Interferon-gamma); FXC9231JVH (Calcitriol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1165/rcmb.2016-0409OC


  9 / 39211 MEDLINE  
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[PMID]:28456076
[Au] Autor:Yang Z; Xu M; Jia Z; Zhang Y; Wang L; Zhang H; Wang J; Song M; Zhao Y; Wu Z; Zhao L; Yin Z; Hong Z
[Ad] Endereço:National Key Laboratory of Medical Chemical Biology & Tianjin Key Laboratory of Protein Science, Nankai University, Tianjin, 300071, China.
[Ti] Título:A novel antigen delivery system induces strong humoral and CTL immune responses.
[So] Source:Biomaterials;134:51-63, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:New strategies with the ability to enhance both the humoral and cellular immune responses remain a priority for the development of future therapeutic cancer vaccines. In this study, we took advantage of ß-glucan particles (GPs) derived from Saccharomyces cerevisiae baker's yeast and a novel reverse micro-emulsion method to prepare an antigen-loaded GP carrier system for dendritic cell (DC) specific antigen delivery, followed by careful evaluation of the immune functions of the prepared particles in initiating both the humoral and cellular immune responses through in vitro and in vivo experiments. The prepared particles greatly promoted DC activation and cytokine production and cross presented the antigen to CD8 cells, inducing very strong OVA specific humoral and cellular immune responses. Treatment with these particles significantly prevented the growth of implanted EG7-OVA tumors in a prophylactic and pre-established tumor model. These results suggest that our strategy may be able to be utilized as a promising platform for cancer immunotherapy.
[Mh] Termos MeSH primário: Imunidade Celular/fisiologia
Imunidade Humoral/fisiologia
Neoplasias/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos/administração & dosagem
Antígenos/imunologia
Vacinas Anticâncer/imunologia
Células Dendríticas/imunologia
Imunoterapia/métodos
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Cancer Vaccines)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  10 / 39211 MEDLINE  
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[PMID]:29360858
[Au] Autor:Zhang A; Yang X; Li Q; Yang Y; Zhao G; Wang B; Wu D
[Ad] Endereço:Xinjiang Key Lab of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
[Ti] Título:Immunostimulatory activity of water-extractable polysaccharides from Cistanche deserticola as a plant adjuvant in vitro and in vivo.
[So] Source:PLoS One;13(1):e0191356, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A safe and effective vaccine adjuvant is important in modern vaccines. Various Chinese herbal polysaccharides can activate the immune system. Cistanche deserticola (CD) is a traditional Chinese herb and an adjuvant candidate. Here, we confirmed that water-extractable polysaccharides of CD (WPCD) could modulate immune responses in vitro and in vivo. In a dose-dependent manner, WPCD significantly promoted the maturation and function of murine marrow-derived dendritic cells (BM-DCs) through up-regulating the expression levels of MHC-II, CD86, CD80, and CD40, allogenic T cell proliferation, and the yields of IL-12 and TNF-α via toll-like receptor4 (TLR4), as indicated by in vitro experiments. In addition, its immunomodulatory activity was also observed in mice. WPCD effectively improved the titers of IgG, IgG1 and IgG2a and markedly enhanced the proliferation of T and B cells, the production of IFN-γ and IL-4 in CD4+ T cells and the expression level of IFN-γ in CD8+ T cells better than Alum. Furthermore, WPCD could markedly up-regulate the expression levels of CD40 and CD80 on DCs in spleen and down-regulate the Treg frequency. The study suggests that polysaccharides of Cistanche deserticola are a safe and effective vaccine adjuvant for eliciting both humoral immunity and cellular immunity by activating DCs via TLR4 signaling pathway.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Cistanche/química
Polissacarídeos/farmacologia
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/administração & dosagem
Adjuvantes Imunológicos/isolamento & purificação
Animais
Diferenciação Celular/efeitos dos fármacos
Células Dendríticas/citologia
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Medicamentos de Ervas Chinesas/administração & dosagem
Medicamentos de Ervas Chinesas/farmacologia
Feminino
Imunidade Celular/efeitos dos fármacos
Imunidade Humoral/efeitos dos fármacos
Imunogenicidade da Vacina/efeitos dos fármacos
Técnicas In Vitro
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos ICR
Ovalbumina/administração & dosagem
Ovalbumina/imunologia
Plantas Medicinais/química
Polissacarídeos/administração & dosagem
Polissacarídeos/isolamento & purificação
Solubilidade
Linfócitos T Reguladores/efeitos dos fármacos
Linfócitos T Reguladores/imunologia
Receptor 4 Toll-Like/metabolismo
Água
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Drugs, Chinese Herbal); 0 (Polysaccharides); 0 (Tlr4 protein, mouse); 0 (Toll-Like Receptor 4); 059QF0KO0R (Water); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191356



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