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Pesquisa : D12.776.543.750.705.852.420.580.750 [Categoria DeCS]
Referências encontradas : 26 [refinar]
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  1 / 26 MEDLINE  
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[PMID]:26104769
[Au] Autor:Sun R; Jia F; Liang Y; Li L; Bai P; Yuan F; Gao L; Zhang L
[Ad] Endereço:Department of Immunology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan, 610041, People's Republic of China. 64366120@qq.com.
[Ti] Título:Interaction analysis of IL-12A and IL-12B polymorphisms with the risk of colorectal cancer.
[So] Source:Tumour Biol;36(12):9295-301, 2015 Dec.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-12 is an antitumor cytokine with functions of inhibiting tumor growth, invasion, and metastasis, indicating that IL-12 is a promising candidate for cancer treatment. The aim of this study was to investigate the association of IL-12A rs568408, IL-12A rs2243115, and IL-12B rs3212227 with the susceptibility to colorectal cancer (CRC). Two hundred and fifty-seven histopathologically confirmed CRC patients and 236 age- and gender-matched controls were enrolled. The three polymorphisms were genotyped using a polymerase chain reaction-restriction fragment length polymorphism assay. We found that the IL-12A rs568408 AG/AA genotypes were associated with an increased risk of CRC with an adjusted odds ratio (OR) of 1.66 (95 % confidence interval (CI), 1.11-2.48). Stratified analyses showed that patients carrying the IL-12B rs3212227AC/CC genotypes had a 1.97-fold increased risk of tumor metastasis (OR = 1.97; 95 % CI, 1.04-3.70). Gene-gene interaction analysis showed that subjects carrying the IL-12A rs568408AG/AA and IL-12B rs3212227AA genotypes had a 2.40-fold increased risk of CRC (OR = 2.40; 95 % CI, 1.14-5.07) and individuals carrying the IL-12A rs568408AG/AA and IL-12B rs3212227AC/CC genotypes had a 1.93-fold increased risk of CRC (OR = 1.93; 95 % CI, 1.10-3.41). These findings indicate that IL-12A rs568408 and IL-12B rs3212227 may be related to the development of CRC.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Predisposição Genética para Doença
Subunidade beta 2 de Receptor de Interleucina-12/genética
Subunidade p40 da Interleucina-12/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Alelos
Grupo com Ancestrais do Continente Asiático
Neoplasias Colorretais/patologia
Feminino
Estudos de Associação Genética
Genótipo
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL12B protein, human); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Interleukin-12 Subunit p40)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150625
[St] Status:MEDLINE
[do] DOI:10.1007/s13277-015-3685-7


  2 / 26 MEDLINE  
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[PMID]:25312725
[Au] Autor:Bobryshev YV; Sobenin IA; Orekhov AN; Chistiakov DA
[Ti] Título:Novel anti-inflammatory interleukin-35 as an emerging target for antiatherosclerotic therapy.
[So] Source:Curr Pharm Des;21(9):1147-51, 2015.
[Is] ISSN:1873-4286
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Atherosclerosis has been widely recognized as a slow progressing inflammatory disease of the aorta and other large caliber arterial vessels. Accumulating evidence suggest that interleukin (IL)-35 can represent an attractive target for future anti-atherosclerotic therapy due to several atheroprotective properties. First, immunosuppressive and anti-inflammatory activity of this cytokine could be beneficial against vascular inflammation. Second, IL-35 can suppress a variety of T cells including proinflammatory Th1 and Th17 cells and probably dendritic cells. Third, IL-35 supports proliferation of regulatory T cells (Tregs), increases their inhibitory function, and induces a new set of Tregs called inducible IL-35-producing Tregs (iTr35 cells). Fourth, this cytokine promotes production of antiinflammatory cytokines such as IL-10 and down-regulates expression of proinflammatory cytokines such as IL-17. Finally, IL-35 is inducible. The fact that IL-35 could be induced by simple compounds such as chemical chaperons may provide advances in developing new efficient strategies for treatment of atherosclerosis. However, it is necessary to test IL-35-inducing factors in order to understand mechanisms of induction and then select the most optimal one. Probably, constructing of humanized antibodies that mimic IL-35 function may provide benefits for advanced atheroprotective therapy.
[Mh] Termos MeSH primário: Aterosclerose/tratamento farmacológico
Mediadores da Inflamação/metabolismo
Interleucinas/metabolismo
Terapia de Alvo Molecular/métodos
[Mh] Termos MeSH secundário: Seres Humanos
Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Interleucinas/biossíntese
Modelos Imunológicos
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Interleukins); 0 (interleukin-35, human)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150107
[Lr] Data última revisão:
150107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141015
[St] Status:MEDLINE


  3 / 26 MEDLINE  
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[PMID]:24743305
[Au] Autor:Wang RX; Yu CR; Dambuza IM; Mahdi RM; Dolinska MB; Sergeev YV; Wingfield PT; Kim SH; Egwuagu CE
[Ad] Endereço:1] Molecular Immunology Section, Laboratory of Immunology, National Eye Institute (NEI), National Institutes of Health (NIH), Bethesda, Maryland, USA. [2] Laboratory of Immunology, Institute of Basic Medical Sciences, Beijing, China.
[Ti] Título:Interleukin-35 induces regulatory B cells that suppress autoimmune disease.
[So] Source:Nat Med;20(6):633-41, 2014 Jun.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin-10 (IL-10)-producing regulatory B (Breg) cells suppress autoimmune disease, and increased numbers of Breg cells prevent host defense to infection and promote tumor growth and metastasis by converting resting CD4(+) T cells to regulatory T (Treg) cells. The mechanisms mediating the induction and development of Breg cells remain unclear. Here we show that IL-35 induces Breg cells and promotes their conversion to a Breg subset that produces IL-35 as well as IL-10. Treatment of mice with IL-35 conferred protection from experimental autoimmune uveitis (EAU), and mice lacking IL-35 (p35 knockout (KO) mice) or defective in IL-35 signaling (IL-12Rß2 KO mice) produced less Breg cells endogenously or after treatment with IL-35 and developed severe uveitis. Adoptive transfer of Breg cells induced by recombinant IL-35 suppressed EAU when transferred to mice with established disease, inhibiting pathogenic T helper type 17 (TH17) and TH1 cells while promoting Treg cell expansion. In B cells, IL-35 activates STAT1 and STAT3 through the IL-35 receptor comprising the IL-12Rß2 and IL-27Rα subunits. As IL-35 also induced the conversion of human B cells into Breg cells, these findings suggest that IL-35 may be used to induce autologous Breg and IL-35(+) Breg cells and treat autoimmune and inflammatory disease.
[Mh] Termos MeSH primário: Transferência Adotiva/métodos
Doenças Autoimunes/tratamento farmacológico
Linfócitos B Reguladores/metabolismo
Interleucinas/farmacologia
Uveíte/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Western Blotting
Imunoprecipitação da Cromatina
Primers do DNA/genética
Engenharia Genética
Imunoprecipitação
Interleucina-10/metabolismo
Subunidade beta 2 de Receptor de Interleucina-12/genética
Interleucinas/administração & dosagem
Interleucinas/genética
Interleucinas/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Reação em Cadeia da Polimerase em Tempo Real
Proteínas Recombinantes/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (DNA Primers); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Interleukins); 0 (Recombinant Proteins); 0 (interleukin-35, mouse); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140419
[St] Status:MEDLINE
[do] DOI:10.1038/nm.3554


  4 / 26 MEDLINE  
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[PMID]:22960221
[Au] Autor:Koch MA; Thomas KR; Perdue NR; Smigiel KS; Srivastava S; Campbell DJ
[Ad] Endereço:Benaroya Research Institute, Seattle, WA 98101, USA.
[Ti] Título:T-bet(+) Treg cells undergo abortive Th1 cell differentiation due to impaired expression of IL-12 receptor ß2.
[So] Source:Immunity;37(3):501-10, 2012 Sep 21.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Foxp3(+) regulatory T (Treg) cells limit inflammatory responses and maintain immune homeostasis. Although comprised of several phenotypically and functionally distinct subsets, the differentiation of specialized Treg cell populations within the periphery is poorly characterized. We demonstrate that the development of T-bet(+) Treg cells that potently inhibit T helper 1 (Th1) cell responses was dependent on the transcription factor STAT1 and occurred directly in response to interferon-γ produced by effector T cells. Additionally, delayed induction of the IL-12Rß2 receptor component after STAT1 activation helped ensure that Treg cells do not readily complete STAT4-dependent Th1 cell development and lose their ability to suppress effector T cell proliferation. Thus, we define a pathway of abortive Th1 cell development that results in the specialization of peripheral Treg cells and demonstrate that impaired expression of a single cytokine receptor helps maintain Treg cell-suppressive function in the context of inflammatory Th1 cell responses.
[Mh] Termos MeSH primário: Diferenciação Celular
Subunidade beta 2 de Receptor de Interleucina-12/imunologia
Linfócitos T Reguladores/imunologia
Células Th1/imunologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Citometria de Fluxo
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/imunologia
Fatores de Transcrição Forkhead/metabolismo
Interferon gama/genética
Interferon gama/metabolismo
Interferon gama/farmacologia
Interleucina-12/farmacologia
Subunidade beta 2 de Receptor de Interleucina-12/genética
Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Receptores CXCR3/genética
Receptores CXCR3/imunologia
Receptores CXCR3/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição STAT1/genética
Fator de Transcrição STAT1/imunologia
Fator de Transcrição STAT1/metabolismo
Fator de Transcrição STAT4/imunologia
Fator de Transcrição STAT4/metabolismo
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/imunologia
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/imunologia
Proteínas com Domínio T-Box/metabolismo
Linfócitos T Reguladores/metabolismo
Células Th1/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cxcr3 protein, mouse); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Receptors, CXCR3); 0 (STAT1 Transcription Factor); 0 (STAT4 Transcription Factor); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 187348-17-0 (Interleukin-12); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120911
[St] Status:MEDLINE


  5 / 26 MEDLINE  
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[PMID]:22343631
[Au] Autor:Pore D; Mahata N; Chakrabarti MK
[Ad] Endereço:Division of Pathophysiology, National Institute of Cholera and Enteric Diseases, P-33, C.I.T. Road, Scheme-XM, Beliaghata, Kolkata 700010, West Bengal, India.
[Ti] Título:Outer membrane protein A (OmpA) of Shigella flexneri 2a links innate and adaptive immunity in a TLR2-dependent manner and involvement of IL-12 and nitric oxide.
[So] Source:J Biol Chem;287(15):12589-601, 2012 Apr 06.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We determine that OmpA of Shigella flexneri 2a is recognized by TLR2 and consequently mediates the release of proinflammatory cytokines and activates NF-κB in HEK 293 cells transfected with TLR2. We also observe that in RAW macrophages TLR2 is essential to instigate the early immune response to OmpA via NF-κB activation and secretion of cytokines and NO. Consistent with these results, TLR2 knockdown using siRNA abolishes the initiation of immune responses. Processing and presentation of OmpA depend on TLR2; MHCII presentation of the processed antigen and expression of CD80 significantly attenuated in TLR2 knockdown macrophages. The optimum production of IFN-γ by the macrophages:CD4(+) T cells co-culture depends on both TLR2 activation and antigen presentation. So, TLR2 is clearly recognized as a decisive factor in initiating host innate immune response to OmpA for the development of CD4(+) T cell adaptive response. Furthermore, we demonstrate in vivo that intranasal immunization of mice with OmpA selectively enhances the release of IFN-γ and IL-2 by CD4(+) T cells. Importantly, OmpA increases the level of IFN-γ production in Ag-primed splenocytes. The addition of neutralizing anti-IL-12p70 mAb to cell cultures results in the decreased release of OmpA-enhanced IFN-γ by Ag-primed splenocytes. Moreover, coincubation with OmpA-pretreated macrophages enhances the production of IFN-γ by OmpA-primed CD4(+) T cells, representing that OmpA may enhance IFN-γ expression in CD4(+) T cells through the induction of IL-12 production in macrophages. These results demonstrate that S. flexneri 2a OmpA may play a critical role in the development of Th1 skewed adaptive immune response.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Proteínas da Membrana Bacteriana Externa/imunologia
Imunidade Inata
Interleucina-12/fisiologia
Óxido Nítrico/metabolismo
Shigella flexneri/fisiologia
Receptor 2 Toll-Like/fisiologia
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno
Ativação Enzimática
Feminino
Células HEK293
Antígenos de Histocompatibilidade Classe II/genética
Antígenos de Histocompatibilidade Classe II/metabolismo
Interações Hospedeiro-Patógeno
Seres Humanos
Interferon gama/biossíntese
Interleucina-12/metabolismo
Subunidade beta 2 de Receptor de Interleucina-12/genética
Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Ativação Linfocitária
Macrófagos/enzimologia
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
NF-kappa B/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Fosforilação
Proteína Quinase C-alfa/metabolismo
Transporte Proteico
Receptores de Quimiocinas/metabolismo
Shigella flexneri/imunologia
Linfócitos T/imunologia
Linfócitos T/metabolismo
Receptor 2 Toll-Like/genética
Receptor 2 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Outer Membrane Proteins); 0 (Histocompatibility Antigens Class II); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (NF-kappa B); 0 (Receptors, Chemokine); 0 (Tlr2 protein, mouse); 0 (Toll-Like Receptor 2); 149024-69-1 (OMPA outer membrane proteins); 187348-17-0 (Interleukin-12); 31C4KY9ESH (Nitric Oxide); 82115-62-6 (Interferon-gamma); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 2.7.11.13 (Protein Kinase C-alpha)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:150225
[Lr] Data última revisão:
150225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120221
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M111.335554


  6 / 26 MEDLINE  
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[PMID]:22265841
[Au] Autor:Meng X; Guo A; Gong W; Jia W; Luo X; Zhai J; Dou Y; Cai X
[Ad] Endereço:State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Animal Virology of Ministry of Agriculture, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Xujiaping 1, Yanchangpu, Chengguan District, Lanzhou 730046, China.
[Ti] Título:Molecular characterization, tissue distribution and expression analysis of interleukin-12 receptor ß2 chain in sheep.
[So] Source:Gene;499(1):124-9, 2012 May 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Ovine ß2 subunit of the interleukin (IL)-12 receptor (IL-12Rß2) was cloned from mRNA preparation of mitogen-activated peripheral blood mononuclear cells (PBMCs). The complete coding sequence for ovine IL-12 Rß2 was found to be 2586 nucleotides in length encoding 862-amino-acid residue protein. It showed 96.4% homology at the nucleotide level and 94.1% homology at the amino acid level with bovine IL-12 Rß2. The ovine IL-12 Rß2 subunit shares common structural and functional elements with their counterparts from the other species. Phylogenetic tree showed that ovine IL-12Rß2 was clustered into the Artiodactyla group, together with those of cattle and pig, which was distinct from the other groups. Real-time RT-PCR was used to investigate expression of the IL-12Rß2 in different tissues of sheep in order to determine the characterization of this receptor in tissue. Expression analysis showed that IL-12Rß2 mRNA expression was detected at all the detected tissues with the exception of thymus.
[Mh] Termos MeSH primário: Subunidade beta 2 de Receptor de Interleucina-12/genética
Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Ovinos/genética
Ovinos/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Bovinos
Células Cultivadas
Clonagem Molecular
Perfilação da Expressão Gênica
Subunidade beta 2 de Receptor de Interleucina-12/química
Subunidade beta 2 de Receptor de Interleucina-12/isolamento & purificação
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/metabolismo
Modelos Moleculares
Dados de Sequência Molecular
Filogenia
RNA Mensageiro/análise
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Homologia de Sequência de Aminoácidos
Ovinos/sangue
Suínos
Timo/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-12 Receptor beta 2 Subunit); 0 (RNA, Messenger)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:120416
[Lr] Data última revisão:
120416
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120124
[St] Status:MEDLINE
[do] DOI:10.1016/j.gene.2011.12.012


  7 / 26 MEDLINE  
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[PMID]:22238458
[Au] Autor:Fauconnier M; Palomo J; Bourigault ML; Meme S; Szeremeta F; Beloeil JC; Danneels A; Charron S; Rihet P; Ryffel B; Quesniaux VF
[Ad] Endereço:Immunologie et Embryologie Moléculaires, Centre National de la Recherche Scientifique, 45071 Orléans, France.
[Ti] Título:IL-12Rß2 is essential for the development of experimental cerebral malaria.
[So] Source:J Immunol;188(4):1905-14, 2012 Feb 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A Th1 response is required for the development of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM). The role of pro-Th1 IL-12 in malaria is complex and controversial. In this study, we addressed the role of IL-12Rß2 in ECM development. C57BL/6 mice deficient for IL-12Rß2, IL-12p40, or IL-12p35 were analyzed for ECM development after blood-stage PbA infection in terms of ischemia and blood flow by noninvasive magnetic resonance imaging and angiography, T cell recruitment, and gene expression. Without IL-12Rß2, no neurologic sign of ECM developed upon PbA infection. Although wild-type mice developed distinct brain microvascular pathology, ECM-resistant, IL-12Rß2-deficient mice showed unaltered cerebral microcirculation and the absence of ischemia after PbA infection. In contrast, mice deficient for IL-12p40 or IL-12p35 were sensitive to ECM development. The resistance of IL-12Rß2-deficient mice to ECM correlated with reduced recruitment of activated T cells and impaired overexpression of lymphotoxin-α, TNF-α, and IFN-γ in the brain after PbA infection. Therefore, IL-12Rß2 signaling is essential for ECM development but independent from IL-12p40 and IL-12p35. We document a novel link between IL-12Rß2 and lymphotoxin-α, TNF-α, and IFN-γ expression, key cytokines for ECM pathogenesis.
[Mh] Termos MeSH primário: Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Malária Cerebral/imunologia
Plasmodium berghei/imunologia
Células Th1/imunologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/microbiologia
Encéfalo/patologia
Linfócitos T CD8-Positivos/imunologia
Interferon gama/biossíntese
Subunidade beta 2 de Receptor de Interleucina-12/deficiência
Subunidade beta 2 de Receptor de Interleucina-12/genética
Subunidade p35 da Interleucina-12/deficiência
Subunidade p35 da Interleucina-12/genética
Subunidade p35 da Interleucina-12/imunologia
Subunidade p40 da Interleucina-12/deficiência
Subunidade p40 da Interleucina-12/genética
Subunidade p40 da Interleucina-12/imunologia
Ativação Linfocitária/imunologia
Linfotoxina-alfa/biossíntese
Malária Cerebral/parasitologia
Malária Cerebral/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Plasmodium berghei/crescimento & desenvolvimento
Plasmodium berghei/patogenicidade
Transdução de Sinais/imunologia
Fator de Necrose Tumoral alfa/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Interleukin-12 Subunit p35); 0 (Interleukin-12 Subunit p40); 0 (Lymphotoxin-alpha); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1203
[Cu] Atualização por classe:120206
[Lr] Data última revisão:
120206
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120113
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1101978


  8 / 26 MEDLINE  
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[PMID]:21844875
[Au] Autor:Ferretti E; Montagna D; Di Carlo E; Cocco C; Ribatti D; Ognio E; Sorrentino C; Lisini D; Bertaina A; Locatelli F; Pistoia V; Airoldi I
[Ad] Endereço:Laboratory of Oncology, G. Gaslini Institute, Genova, Italy.
[Ti] Título:Absence of IL-12Rß2 in CD33(+)CD38(+) pediatric acute myeloid leukemia cells favours progression in NOD/SCID/IL2RγC-deficient mice.
[So] Source:Leukemia;26(2):225-35, 2012 Feb.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Childhood acute myeloid leukemia (AML) is a hematological malignancy in which tumor burden is continuously replenished by leukemic-initiating cells (ICs), which proliferate slowly and are refractory to chemotherapeutic agents. We investigated whether interleukin (IL)-12, an immuno-modulatory cytokine with anti-tumor activity, may target AML blasts (CD45(+)CD33(+)) and populations known to contain leukemia ICs (that is, CD34(+)CD38(-), CD33(+)CD38(+) and CD44(+)CD38(-) cells). We demonstrate for the first time that: i) AML blasts and their CD34(+)CD38(-), CD33(+)CD38(+), CD44(+)CD38(-) subsets express the heterodimeric IL-12 receptor (IL-12R), ii) AML cells injected subcutaneously into NOD/SCID/Il2rg(-/-) (NSG) mice developed a localized tumor mass containing leukemic ICs and blasts that were virtually eliminated by IL-12 treatment, iii) AML cells injected intravenously into NSG mice engrafted within the first month in the spleen, but not in bone marrow or peripheral blood. At this time, IL-12 dramatically dampened AML CD45(+)CD33(+), CD34(+)CD38(-), CD33(+)CD38(+) and CD44(+)CD38(-) populations, only sparing residual CD33(+)CD38(+) cells that did not express IL-12Rß2. From 30 to 60 days after the initial inoculum, these IL-12-unresponsive cells expanded and metastasized in both control and IL-12-treated NSG mice. Our data indicate that the absence of IL-12Rß2 in pediatric AML cells favours leukemia progression in NOD/SCID/IL2Rγc-deficient mice.
[Mh] Termos MeSH primário: ADP-Ribosil Ciclase 1/imunologia
Antígenos CD/imunologia
Antígenos de Diferenciação Mielomonocítica/imunologia
Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Leucemia Mieloide Aguda/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Divisão Celular
Criança
Pré-Escolar
Progressão da Doença
Feminino
Citometria de Fluxo
Seres Humanos
Lactente
Leucemia Mieloide Aguda/imunologia
Leucemia Mieloide Aguda/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Reação em Cadeia da Polimerase em Tempo Real
Lectina 3 Semelhante a Ig de Ligação ao Ácido Siálico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (CD33 protein, human); 0 (Cd33 protein, mouse); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Sialic Acid Binding Ig-like Lectin 3); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1203
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110817
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2011.213


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[PMID]:22182694
[Au] Autor:Kress-Bennett JM; Ehrlich GD; Bruno A; Post JC; Hu FZ; Scott TF
[Ad] Endereço:Center for Genomic Sciences, Allegheny-Singer Research Institute, Pittsburgh, PA 15212, USA.
[Ti] Título:Preliminary study: treatment with intramuscular interferon beta-1a results in increased levels of IL-12Rß2+ and decreased levels of IL23R+ CD4+ T - Lymphocytes in multiple sclerosis.
[So] Source:BMC Neurol;11:155, 2011 Dec 19.
[Is] ISSN:1471-2377
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There are a lack of biomarkers which can be used to predict clinical outcomes for multiple sclerosis (MS) patients receiving interferon beta (IFN-ß). Thus the objective of this study was to characterize changes in CD4+ T-lymphocyte expression in an unbiased manner following initiation of intramuscular (IM) IFN-ß-1a treatment, and then to verify those findings using marker-specific assays. METHODS: Peripheral blood specimens were collected from twenty MS patients before and after treatment with intramuscular (IM) IFN-ß-1a and were used for isolation of mononuclear cells (PBMCs). mRNA expression patterns of negatively-selected CD4+ T-cells from the PBMCs were analyzed using microarray gene expression technology. IL-12 and IL-23 receptor levels on PBMC-derived CD4+ T-cells were analyzed by flow cytometry. The phosphorylation status of Stat4 was measured by performing densitometry on western blots. RESULTS: Microarray analyses demonstrated that mRNA expression of the IL-12Rß2 gene was uniformly up-regulated in response to IFN-ß-1a treatment and was associated with an increased number of IL-12Rß2+ CD4+ T-cells by flow cytometry in 4 of 6 patients. This finding was substantiated by demonstrating that Stat4 phosphorylation, a transcription factor for IL-12, was increased after treatment. Conversely, the number of IL-23R+ CD4+ T-cells was decreased following treatment. CONCLUSIONS: The IL-12 receptor shares a common subunit, the IL-12Rß2, with the IL-23 receptor. Both of these receptors have a probable role in regulating IL-17 and TH-17 cells, important mediators of inflammation in multiple sclerosis (MS). Thus, the changes in the numbers of CD4+ T-cells expressing these receptors in response to IFN-ß-1a treatment may point to an important mechanism of action for this drug, but further large scale studies are needed to confirm these preliminary observations.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Interferon beta/administração & dosagem
Subunidade beta 2 de Receptor de Interleucina-12/efeitos dos fármacos
Esclerose Múltipla Recidivante-Remitente/tratamento farmacológico
Esclerose Múltipla Recidivante-Remitente/imunologia
Receptores de Interleucina-12/efeitos dos fármacos
Receptores de Interleucina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/uso terapêutico
Adulto
Contagem de Linfócito CD4
Feminino
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Injeções Intramusculares
Interferon beta-1a
Subunidade beta 2 de Receptor de Interleucina-12/imunologia
Ativação Linfocitária/efeitos dos fármacos
Ativação Linfocitária/genética
Masculino
Meia-Idade
Receptores de Interleucina/imunologia
Receptores de Interleucina-12/imunologia
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (IL23R protein, human); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Receptors, Interleukin); 0 (Receptors, Interleukin-12); 77238-31-4 (Interferon-beta); XRO4566Q4R (Interferon beta-1a)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111221
[St] Status:MEDLINE
[do] DOI:10.1186/1471-2377-11-155


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[PMID]:21748639
[Au] Autor:Marshall NB; Hauck LL; Mourich DV
[Ad] Endereço:Department of Microbiology, Oregon State University, Corvallis, OR, USA. marshaln@onid.orst.edu
[Ti] Título:Five-step process for screening antisense compounds for efficacy: gene target IL-12Rb2.
[So] Source:Methods Mol Biol;764:153-68, 2011.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antisense technologies are widely used for the inhibition of gene expression. Although traditionally the AUG start codon of the open reading frame is targeted to disrupt ribosome assembly and initiation, an emerging approach is targeting sequences to disrupt pre-mRNA splicing. The primary advantage to using this approach is a positive read-out for an antisense effect through detection of a novel splice product, but additional benefit can be found in generating a novel splice product with altered functional properties. The antisense compounds used here are phosphorodiamidate morpholino oligomers conjugated to an arginine-rich cell penetrating peptide (P-PMO). We describe a five-step process for selecting the best candidate antisense compound for altering IL-12Rb2 expression including (1) detecting mRNA splice products by RT-PCR, (2) measuring protein expression, (3) evaluating protein function, (4) checking cellular viability, and (5) validating efficacy of the final candidate compound. The significance of targeting exons composed of a number of base pairs divisible by 3 is also discussed. The five steps described here for selecting the best candidate P-PMO to alter IL-12Rb2 expression should be applied for designing and screening antisense compounds for other gene targets.
[Mh] Termos MeSH primário: Bioensaio
Peptídeos Penetradores de Células/metabolismo
Subunidade beta 2 de Receptor de Interleucina-12/antagonistas & inibidores
Terapia de Alvo Molecular/métodos
Morfolinas/farmacologia
Oligonucleotídeos Antissenso/farmacologia
Precursores de RNA/antagonistas & inibidores
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Arginina/química
Sobrevivência Celular/efeitos dos fármacos
Peptídeos Penetradores de Células/química
Expressão Gênica/efeitos dos fármacos
Interferon gama/genética
Interferon gama/metabolismo
Subunidade beta 2 de Receptor de Interleucina-12/genética
Subunidade beta 2 de Receptor de Interleucina-12/metabolismo
Camundongos
Camundongos Endogâmicos
Morfolinas/química
Morfolinas/metabolismo
Morfolinos
Oligonucleotídeos Antissenso/química
Oligonucleotídeos Antissenso/metabolismo
Fases de Leitura Aberta
Processamento de RNA/efeitos dos fármacos
RNA Mensageiro/antagonistas & inibidores
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição STAT4/genética
Fator de Transcrição STAT4/metabolismo
Linfócitos T/citologia
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell-Penetrating Peptides); 0 (Interleukin-12 Receptor beta 2 Subunit); 0 (Morpholines); 0 (Morpholinos); 0 (Oligonucleotides, Antisense); 0 (RNA Precursors); 0 (RNA, Messenger); 0 (STAT4 Transcription Factor); 82115-62-6 (Interferon-gamma); 94ZLA3W45F (Arginine)
[Em] Mês de entrada:1110
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110713
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-61779-188-8_10



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