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Pesquisa : B01.050.500.500.294.400.968.400.575 [Categoria DeCS]
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  1 / 1086 MEDLINE  
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[PMID]:28747424
[Au] Autor:Schwartz C; Khan AR; Floudas A; Saunders SP; Hams E; Rodewald HR; McKenzie ANJ; Fallon PG
[Ad] Endereço:Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland.
[Ti] Título:ILC2s regulate adaptive Th2 cell functions via PD-L1 checkpoint control.
[So] Source:J Exp Med;214(9):2507-2521, 2017 Sep 04.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group 2 innate lymphoid cells (ILC2s) are important effector cells driving the initiation of type 2 immune responses leading to adaptive T helper 2 (Th2) immunity. Here we show that ILC2s dynamically express the checkpoint inhibitor molecule PD-L1 during type 2 pulmonary responses. Surprisingly, PD-L1:PD-1 interaction between ILC2s and CD4 T cells did not inhibit the T cell response, but PD-L1-expressing ILC2s stimulated increased expression of GATA3 and production of IL-13 by Th2 cells both in vitro and in vivo. Conditional deletion of PD-L1 on ILC2s impaired early Th2 polarization and cytokine production, leading to delayed worm expulsion during infection with the gastrointestinal helminth Our results identify a novel PD-L1-controlled mechanism for type 2 polarization, with ILC2s mediating an innate checkpoint to control adaptive T helper responses, which has important implications for the treatment of type 2 inflammation.
[Mh] Termos MeSH primário: Antígeno B7-H1/fisiologia
Linfócitos/fisiologia
Células Th2/fisiologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa/imunologia
Imunidade Adaptativa/fisiologia
Animais
Antígeno B7-H1/imunologia
Fator de Transcrição GATA3/fisiologia
Imunidade Celular/imunologia
Imunidade Celular/fisiologia
Interleucina-13/fisiologia
Linfócitos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Nippostrongylus/imunologia
Infecções por Strongylida/imunologia
Células Th2/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (Cd274 protein, mouse); 0 (GATA3 Transcription Factor); 0 (Gata3 protein, mouse); 0 (Interleukin-13)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20170051


  2 / 1086 MEDLINE  
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[PMID]:29335213
[Au] Autor:Sugawara A; Kubo M; Hirose T; Yahagi K; Tsunoda N; Noguchi Y; Nakashima T; Takahashi Y; Welz C; Mueller D; Mertens C; Koebberling J; Omura S; Sunazuka T
[Ad] Endereço:Kitasato Institute for Life Sciences and Graduate School of Infection Control Sciences, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan; Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Aza-Aoba, Aramaki, Aoba-ku, Sendai, 980-8578, Japan. Electronic address
[Ti] Título:Jietacins, azoxy antibiotics with potent nematocidal activity: Design, synthesis, and biological evaluation against parasitic nematodes.
[So] Source:Eur J Med Chem;145:524-538, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Jietacins, an azoxy antibiotic class of chemicals, were isolated from the culture broth of Streptomyces sp. KP-197. They have a unique structural motif, including a vinyl azoxy group and a long acyclic aliphatic chain, which is usually branched but non-branched in the case of jietacin C. During a drug discovery program, we found that jietacins display potent anthelmintic activity against parasitic nematodes and that jietacin A has a moderate or low acute toxicity (LD > 300 mg/kg) and no mutagenic potential in a mini Ames screen. This suggests that jietacins have potential for drug discovery research. In order to create a novel anthelmintic agent, we performed design, synthesis, and biological evaluation of jietacin derivatives against parasitic nematodes. Of these derivatives, we found that a fully synthesized simplified derivative exhibited better anthelmintic activity against three parasitic nematodes than natural jietacins. In addition, it had a better efficacy in vivo through oral administration against a mouse nematode. This indicated that the azoxy motif could prove useful as a template for anthelmintic discovery, possibly creating a class of anthelmintic with novel skeletons, a potential new mode of action, and providing further insight for rational drug design.
[Mh] Termos MeSH primário: Anti-Helmínticos/farmacologia
Antibacterianos/farmacologia
Compostos Azo/farmacologia
Desenho de Drogas
Nematoides/efeitos dos fármacos
Nippostrongylus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Anti-Helmínticos/administração & dosagem
Anti-Helmínticos/química
Antibacterianos/administração & dosagem
Antibacterianos/química
Compostos Azo/administração & dosagem
Compostos Azo/química
Relação Dose-Resposta a Droga
Camundongos
Estrutura Molecular
Testes de Sensibilidade Parasitária
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthelmintics); 0 (Anti-Bacterial Agents); 0 (Azo Compounds); 109766-61-2 (jietacin A)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


  3 / 1086 MEDLINE  
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[PMID]:28684424
[Au] Autor:Shay AE; Diwakar BT; Guan BJ; Narayan V; Urban JF; Prabhu KS
[Ad] Endereço:From the Department of Veterinary and Biomedical Sciences, Center for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802.
[Ti] Título:IL-4 up-regulates cyclooxygenase-1 expression in macrophages.
[So] Source:J Biol Chem;292(35):14544-14555, 2017 Sep 01.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macrophages use various cell-surface receptors to sense their environment and undergo polarized responses. The cytokines, interleukin (IL)-4 and IL-13, released from T-helper type 2 (Th2) cells, drive macrophage polarization toward an alternatively activated phenotype (M2). This phenotype is associated with the expression of potent pro-resolving mediators, such as the prostaglandin (PG) D -derived cyclopentenone metabolite, 15d-PGJ , produced by the cyclooxygenase ( ; Cox) pathway. Interestingly, IL-4 treatment of bone marrow-derived macrophages (BMDMs) significantly down-regulates Cox-2 protein expression, whereas Cox-1 levels are significantly increased. This phenomenon not only challenges the dogma that Cox-1 is only developmentally regulated, but also demonstrates a novel mechanism in which IL-4-dependent regulation of Cox-1 involves the activation of the mechanistic target of rapamycin complex (mTORC). Using specific chemical inhibitors, we demonstrate here that IL-4-dependent Cox-1 up-regulation occurs at the post-transcriptional level via the Fes-Akt-mTORC axis. Activation of AMP-activated protein kinase (AMPK) by metformin, inhibition of mTORC by torin 1, or CRISPR/Cas9-mediated genetic knock-out of tuberous sclerosis complex-2 (Tsc2) blocked the IL-4-dependent expression of Cox-1 and the ability of macrophages to polarize to M2. However, use of 15d-PGJ partially rescued the effects of AMPK activation, suggesting the importance of Cox-1 in macrophage polarization as also observed in a model of gastrointestinal helminth clearance. In summary, these findings suggest a new paradigm where IL-4-dependent up-regulation of Cox-1 expression may play a key role in tissue homeostasis and wound healing during Th2-mediated immune responses, such as parasitic infections.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Interleucina-4/metabolismo
Ativação de Macrófagos
Macrófagos/metabolismo
Proteínas de Membrana/agonistas
Modelos Imunológicos
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/química
Animais
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Células da Medula Óssea/metabolismo
Células da Medula Óssea/patologia
Células Cultivadas
Ciclo-Oxigenase 1/genética
Ciclo-Oxigenase 1/metabolismo
Ativação Enzimática/efeitos dos fármacos
Indução Enzimática/efeitos dos fármacos
Inibidores Enzimáticos/farmacologia
Células HEK293
Seres Humanos
Imunomodulação/efeitos dos fármacos
Interleucina-4/genética
Ligantes
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Ativação de Macrófagos/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Macrófagos/patologia
Masculino
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Metformina/farmacologia
Metformina/uso terapêutico
Camundongos Endogâmicos C57BL
Nippostrongylus/efeitos dos fármacos
Nippostrongylus/crescimento & desenvolvimento
Nippostrongylus/imunologia
Prostaglandina D2/análogos & derivados
Prostaglandina D2/metabolismo
Prostaglandina D2/uso terapêutico
Proteínas Recombinantes/metabolismo
Infecções por Strongylida/imunologia
Infecções por Strongylida/metabolismo
Infecções por Strongylida/patologia
Infecções por Strongylida/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (15-deoxyprostaglandin J2); 0 (Enzyme Inhibitors); 0 (Ligands); 0 (Luminescent Proteins); 0 (Membrane Proteins); 0 (Recombinant Proteins); 207137-56-2 (Interleukin-4); 9100L32L2N (Metformin); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Ptgs1 protein, mouse); EC 2.7.11.1 (AMPK alpha1 subunit, mouse); EC 2.7.11.31 (AMP-Activated Protein Kinases); RXY07S6CZ2 (Prostaglandin D2)
[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:170708
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.785014


  4 / 1086 MEDLINE  
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[PMID]:28651009
[Au] Autor:Nono JK; Ndlovu H; Abdel Aziz N; Mpotje T; Hlaka L; Brombacher F
[Ad] Endereço:Cytokines and Diseases Group, International Centre for Genetic Engineering and Biotechnology, Cape Town Component, Cape Town, South Africa.
[Ti] Título:Interleukin-4 receptor alpha is still required after Th2 polarization for the maintenance and the recall of protective immunity to Nematode infection.
[So] Source:PLoS Negl Trop Dis;11(6):e0005675, 2017 Jun.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is currently no vaccine against parasitic nematodes and the knowledge on the mechanisms by which protective immunity against this class of parasites is achieved is continuously expanding. Nematode parasites trigger a host protective type 2 immune response via interleukin-4 receptor alpha (IL-4Rα). Despite this central role, it is not known whether IL-4Rα has a role in maintaining host type 2 immune responses following polarization. To determine the role of IL-4Rα after polarization, we used a recently established strain of rosaCreERT2-/+IL-4Rα-/Lox mice where il4rα gene deletion can be temporally controlled. We show that sustained expression of IL-4Rα is required for the maintenance of type 2 immune responses and protective immunity following interruption after polarization with Nippostrongylus brasiliensis primary infection. Moreover, we show by temporal deletion of IL-4Rα prior to secondary infection with N. brasiliensis that signaling via this receptor drives more efficient recall of type 2 immune responses and clearance of the parasites. Together, this study demonstrates that sustained IL-4Rα mediated signaling is required for the maintenance of anti-nematode type 2 immune responses, describing a novel function for IL-4Rα that is distinct from its role in immune polarization.
[Mh] Termos MeSH primário: Subunidade alfa de Receptor de Interleucina-4/metabolismo
Nippostrongylus/imunologia
Infecções por Strongylida/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Deleção de Genes
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-4 Receptor alpha Subunit)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0005675


  5 / 1086 MEDLINE  
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[PMID]:28490441
[Au] Autor:Taylor S; Huang Y; Mallett G; Stathopoulou C; Felizardo TC; Sun MA; Martin EL; Zhu N; Woodward EL; Elias MS; Scott J; Reynolds NJ; Paul WE; Fowler DH; Amarnath S
[Ad] Endereço:Experimental Transplantation Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
[Ti] Título:PD-1 regulates KLRG1 group 2 innate lymphoid cells.
[So] Source:J Exp Med;214(6):1663-1678, 2017 Jun 05.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group 2 innate lymphoid cells (ILC-2s) regulate immune responses to pathogens and maintain tissue homeostasis in response to cytokines. Positive regulation of ILC-2s through ICOS has been recently elucidated. We demonstrate here that PD-1 is an important negative regulator of KLRG1 ILC-2 function in both mice and humans. Increase in KLRG1 ILC-2 cell numbers was attributed to an intrinsic defect in PD-1 signaling, which resulted in enhanced STAT5 activation. During infection, a significant expansion of KLRG1 ILC-2 subsets occurred in mice and, upon adoptive transfer, KLRG1 ILC-2s significantly reduced worm burden. Furthermore, blocking PD-1 with an antibody increased KLRG1 ILC-2 cell number and reduced disease burden. Therefore, PD-1 is required for maintaining the number, and hence function, of KLRG1 ILC-2s.
[Mh] Termos MeSH primário: Imunidade Inata
Lectinas Tipo C/metabolismo
Linfócitos/metabolismo
Receptor de Morte Celular Programada 1/metabolismo
Receptores Imunológicos/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Animais
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Contagem de Linfócitos
Subpopulações de Linfócitos/metabolismo
Camundongos Endogâmicos C57BL
Nippostrongylus/fisiologia
Parasitos/fisiologia
Receptor de Morte Celular Programada 1/deficiência
Fator de Transcrição STAT5/metabolismo
Transdução de Sinais
Infecções por Strongylida/imunologia
Infecções por Strongylida/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (KLRG1 protein, human); 0 (Klrg1 protein, mouse); 0 (Lectins, C-Type); 0 (PDCD1 protein, human); 0 (Pdcd1 protein, mouse); 0 (Programmed Cell Death 1 Receptor); 0 (Receptors, Immunologic); 0 (STAT5 Transcription Factor); 0 (Trans-Activators); 128559-51-3 (RAG-1 protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161653


  6 / 1086 MEDLINE  
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[PMID]:28402847
[Au] Autor:Spadaro O; Camell CD; Bosurgi L; Nguyen KY; Youm YH; Rothlin CV; Dixit VD
[Ad] Endereço:Section of Comparative Medicine and Program on Integrative Cell Signaling and Neurobiology of Metabolism, Yale School of Medicine, New Haven, CT 06520, USA; Department of Immunobiology, Yale School of Medicine, New Haven, CT 06520, USA.
[Ti] Título:IGF1 Shapes Macrophage Activation in Response to Immunometabolic Challenge.
[So] Source:Cell Rep;19(2):225-234, 2017 Apr 11.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In concert with their phagocytic activity, macrophages are thought to regulate the host immunometabolic responses primarily via their ability to produce specific cytokines and metabolites. Here, we show that IL-4-differentiated, M2-like macrophages secrete IGF1, a hormone previously thought to be exclusively produced from liver. Ablation of IGF1 receptors from myeloid cells reduced phagocytosis, increased macrophages in adipose tissue, elevated adiposity, lowered energy expenditure, and led to insulin resistance in mice fed a high-fat diet. The investigation of adipose macrophage phenotype in obese myeloid IGF1R knockout (MIKO) mice revealed a reduction in transcripts associated with M2-like macrophage activation. Furthermore, the MIKO mice infected with helminth Nippostrongylus brasiliensis displayed delayed resolution from infection with normal insulin sensitivity. Surprisingly, cold challenge did not trigger an overt M2-like state and failed to induce tyrosine hydroxylase expression in adipose tissue macrophages of control or MIKO mice. These results show that IGF1 signaling shapes the macrophage-activation phenotype.
[Mh] Termos MeSH primário: Resistência à Insulina/genética
Fator de Crescimento Insulin-Like I/genética
Macrófagos/imunologia
Infecções por Strongylida/imunologia
[Mh] Termos MeSH secundário: Tecido Adiposo/imunologia
Tecido Adiposo/metabolismo
Adiposidade
Animais
Diferenciação Celular/imunologia
Dieta Hiperlipídica
Resistência à Insulina/imunologia
Fator de Crescimento Insulin-Like I/imunologia
Interleucina-4/imunologia
Macrófagos/metabolismo
Camundongos
Camundongos Knockout
Nippostrongylus/patogenicidade
Fagocitose/genética
Transdução de Sinais/imunologia
Infecções por Strongylida/metabolismo
Infecções por Strongylida/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (insulin-like growth factor-1, mouse); 207137-56-2 (Interleukin-4); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170414
[St] Status:MEDLINE


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[PMID]:27977850
[Au] Autor:Entwistle LJ; Wilson MS
[Ad] Endereço:Allergy and Anti-Helminth Laboratory, The Francis Crick Institute, London, UK.
[Ti] Título:MicroRNA-mediated regulation of immune responses to intestinal helminth infections.
[So] Source:Parasite Immunol;39(2), 2017 Feb.
[Is] ISSN:1365-3024
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Intestinal helminth infections are highly prevalent in the developing world, often resulting in chronic infection and inflicting high host morbidity. With the emergence of drug-resistant parasites, a limited number of chemotherapeutic drugs available and stalling vaccine efforts, an increased understanding of antihelminth immunity is essential to provide new avenues to therapeutic intervention. MicroRNAs are a class of small, nonprotein coding RNAs which negatively regulate mRNA translation, thus providing finite control over gene expression in a plethora of biological settings. The miRNA-mediated coordinated control of gene expression has been shown to be essential in infection and immunity, in promoting and fine-tuning the appropriate immune response. This review gathers together and discusses observations of miRNA-mediated effects on the immune system and the subsequent impact on our understanding of antihelminth immunity.
[Mh] Termos MeSH primário: Imunidade Adaptativa/genética
Imunidade Adaptativa/imunologia
Helmintíase/imunologia
Enteropatias Parasitárias/imunologia
Mucosa Intestinal/imunologia
MicroRNAs/genética
Infecções por Strongylida/imunologia
Triquinelose/imunologia
Tricuríase/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/imunologia
Células Dendríticas/imunologia
Modelos Animais de Doenças
Helmintíase/parasitologia
Enteropatias Parasitárias/parasitologia
Mucosa Intestinal/parasitologia
Camundongos
Nematospiroides dubius/imunologia
Nippostrongylus/imunologia
Infecções por Strongylida/parasitologia
Trichinella spiralis/imunologia
Triquinelose/parasitologia
Tricuríase/parasitologia
Trichuris/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161216
[St] Status:MEDLINE
[do] DOI:10.1111/pim.12406


  8 / 1086 MEDLINE  
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[PMID]:27913566
[Au] Autor:Connor LM; Tang SC; Cognard E; Ochiai S; Hilligan KL; Old SI; Pellefigues C; White RF; Patel D; Smith AA; Eccles DA; Lamiable O; McConnell MJ; Ronchese F
[Ad] Endereço:Malaghan Institute of Medical Research, Wellington 6012, New Zealand.
[Ti] Título:Th2 responses are primed by skin dendritic cells with distinct transcriptional profiles.
[So] Source:J Exp Med;214(1):125-142, 2017 Jan.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The dendritic cell signals required for the in vivo priming of IL-4-producing T cells are unknown. We used RNA sequencing to characterize DCs from skin LN of mice exposed to two different Th2 stimuli: the helminth parasite Nippostrongylus brasiliensis (Nb) and the contact sensitizer dibutyl phthalate (DBP)-FITC. Both Nb and DBP-FITC induced extensive transcriptional changes that involved multiple DC subsets. Surprisingly, these transcriptional changes were highly distinct in the two models, with only a small number of genes being similarly regulated in both conditions. Pathway analysis of expressed genes identified no shared pathways between Nb and DBP-FITC, but revealed a type-I IFN (IFN-I) signature unique to DCs from Nb-primed mice. Blocking the IFN-I receptor at the time of Nb treatment had little effect on DC migration and antigen transport to the LN, but inhibited the up-regulation of IFN-I-induced markers on DCs and effectively blunted Th2 development. In contrast, the response to DBP-FITC was not affected by IFN-I receptor blockade, a finding consistent with the known dependence of this response on the innate cytokine TSLP. Thus, the priming of Th2 responses is associated with distinct transcriptional signatures in DCs in vivo, reflecting the diverse environments in which Th2 immune responses are initiated.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Pele/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Animais
Imunoglobulinas/fisiologia
Interferon Tipo I/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Nippostrongylus/imunologia
Receptor de Interferon alfa e beta/fisiologia
Receptores de Citocinas/fisiologia
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ifnar1 protein, mouse); 0 (Immunoglobulins); 0 (Interferon Type I); 0 (Receptors, Cytokine); 0 (Tslpr protein, mouse); 156986-95-7 (Receptor, Interferon alpha-beta)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20160470


  9 / 1086 MEDLINE  
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[PMID]:27049059
[Au] Autor:Damle SR; Martin RK; Cross JV; Conrad DH
[Ad] Endereço:Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298.
[Ti] Título:Macrophage migration inhibitory factor deficiency enhances immune response to Nippostrongylus brasiliensis.
[So] Source:Mucosal Immunol;10(1):205-214, 2017 Jan.
[Is] ISSN:1935-3456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infections with helminth parasites are endemic in the developing world and are a target for intervention with new therapies. Macrophage migration inhibitory factor (MIF) is a cytokine with pleiotropic effects in inflammation and immune responses. We investigated the role of MIF in a naturally cleared model of helminth infection in rodents, Nippostrongylus brasiliensis. At day 7 postinfection, MIF-deficient (MIF ) mice had reduced parasite burden and mounted an enhanced type 2 immune response (Th2), including increased Gata3 expression and interleukin-13 (IL-13) production in the mesenteric lymph nodes (MLNs). Bone marrow reconstitution demonstrated that MIF produced from hematopoietic cells was crucial and Rag1 reconstitution provided direct evidence that MIF CD4 T cells were responsible for the augmented parasite clearance. MIF CD4 T cells produced less IL-6 postinfection, which correlated with enhanced Th2 responses. MIF CD4 T cells exhibited lower nuclear factor-κB activation, potentially explaining the reduction in IL-6. Finally, we demonstrated enhanced clearance of the parasite and Th2 response in wild-type mice treated with the MIF tautomerase inhibitor, sulforaphane, a compound found naturally found in cruciferous vegetables. These results are the first to describe the importance of the tautomerase enzyme activity in MIF function in N. brasiliensis infection.
[Mh] Termos MeSH primário: Fator de Transcrição GATA3/metabolismo
Interleucina-13/metabolismo
Oxirredutases Intramoleculares/metabolismo
Fatores Inibidores da Migração de Macrófagos/metabolismo
Macrófagos/imunologia
Nippostrongylus/imunologia
Infecções por Strongylida/imunologia
Células Th2/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Helmintos/imunologia
Células Cultivadas
Feminino
Fator de Transcrição GATA3/genética
Imunidade
Oxirredutases Intramoleculares/antagonistas & inibidores
Oxirredutases Intramoleculares/genética
Isotiocianatos/uso terapêutico
Fatores Inibidores da Migração de Macrófagos/genética
Macrófagos/parasitologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Carga Parasitária
Infecções por Strongylida/tratamento farmacológico
Células Th2/efeitos dos fármacos
Células Th2/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Helminth); 0 (GATA3 Transcription Factor); 0 (Gata3 protein, mouse); 0 (Interleukin-13); 0 (Isothiocyanates); 0 (Macrophage Migration-Inhibitory Factors); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.2.1 (Mif protein, mouse); EC 5.3.3.12 (dopachrome isomerase); GA49J4310U (sulforafan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160407
[St] Status:MEDLINE
[do] DOI:10.1038/mi.2016.29


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[PMID]:28095659
[Au] Autor:Chaudhary A; Goswami U; Singh HS
[Ad] Endereço:Molecular Taxonomy Laboratory, Department of Zoology, Chaudhary Charan Singh University, Meerut (U.P.), 250004, India.
[Ti] Título:Molecular Characterization of (Nematoda: Heligmosomatidae) from in India.
[So] Source:Korean J Parasitol;54(6):743-750, 2016 Dec.
[Is] ISSN:1738-0006
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:(Rodentia: Muridae) has generally been infected with a rodent hookworm . In this report, we present morphological and molecular identification of by light and scanning electron microscopy and PCR amplification of mitochondrial cytochrome c oxidase subunit 1 ( ) gene and the protein sequences encoded by gene, respectively. Despite the use of in many biochemistry studies from India, their taxonomic identification was not fully understood, especially at the species level, and no molecular data is available in GenBank from India. Sequence analysis of gene in this study revealed that the present specimen showed close identity with the same species available in GenBank, confirming that the species is . This study represents the first record of molecular identification of from India and the protein structure to better understand the comparative phylogenetic characteristics.
[Mh] Termos MeSH primário: Nippostrongylus/classificação
Nippostrongylus/isolamento & purificação
Doenças dos Roedores/parasitologia
Infecções por Strongylida/veterinária
[Mh] Termos MeSH secundário: Estruturas Animais/anatomia & histologia
Animais
Análise por Conglomerados
DNA de Helmintos/química
DNA de Helmintos/genética
Complexo IV da Cadeia de Transporte de Elétrons/genética
Feminino
Índia
Masculino
Camundongos
Microscopia
Nippostrongylus/anatomia & histologia
Nippostrongylus/genética
Filogenia
Análise de Sequência de DNA
Infecções por Strongylida/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Helminth); EC 1.9.3.1 (Electron Transport Complex IV)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170414
[Lr] Data última revisão:
170414
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.3347/kjp.2016.54.6.743



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