Base de dados : MEDLINE
Pesquisa : D12.776.543.750.705.852.420.820 [Categoria DeCS]
Referências encontradas : 556 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 56 ir para página                         

  1 / 556 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29329326
[Au] Autor:Ting JP; Tung F; Antonysamy S; Wasserman S; Jones SB; Zhang FF; Espada A; Broughton H; Chalmers MJ; Woodman ME; Bina HA; Dodge JA; Benach J; Zhang A; Groshong C; Manglicmot D; Russell M; Afshar S
[Ad] Endereço:Department of protein Engineering, Eli Lilly Biotechnology Center, San Diego, California, United States of America.
[Ti] Título:Utilization of peptide phage display to investigate hotspots on IL-17A and what it means for drug discovery.
[So] Source:PLoS One;13(1):e0190850, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To date, IL-17A antibodies remain the only therapeutic approach to correct the abnormal activation of the IL-17A/IL-17R signaling complex. Why is it that despite the remarkable success of IL-17 antibodies, there is no small molecule antagonist of IL-17A in the clinic? Here we offer a unique approach to address this question. In order to understand the interaction of IL-17A with its receptor, we combined peptide discovery using phage display with HDX, crystallography, and functional assays to map and characterize hot regions that contribute to most of the energetics of the IL-17A/IL-17R interaction. These functional maps are proposed to serve as a guide to aid in the development of small molecules that bind to IL-17A and block its interaction with IL-17RA.
[Mh] Termos MeSH primário: Colífagos/metabolismo
Interleucina-17/metabolismo
Peptídeos/metabolismo
Receptores de Interleucina-17/metabolismo
[Mh] Termos MeSH secundário: Cristalografia por Raios X
Ensaio de Imunoadsorção Enzimática
Células HT29
Seres Humanos
Interleucina-17/química
Modelos Moleculares
Receptores de Interleucina-17/química
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-17); 0 (Peptides); 0 (Receptors, Interleukin-17)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190850


  2 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27773660
[Au] Autor:Al-Harbi NO; Nadeem A; Al-Harbi MM; Zoheir KMA; Ansari MA; El-Sherbeeny AM; Alanazi KM; Alotaibi MR; Ahmad SF
[Ad] Endereço:Department of Pharmacology & Toxicology, College of Pharmacy, Riyadh, Saudi Arabia.
[Ti] Título:Psoriatic inflammation causes hepatic inflammation with concomitant dysregulation in hepatic metabolism via IL-17A/IL-17 receptor signaling in a murine model.
[So] Source:Immunobiology;222(2):128-136, 2017 02.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Psoriatic inflammation has been shown to be associated with cardiovascular dysfunction and systemic inflammation. Recently, psoriasis has also been linked to hepatic disorders, however underlying mechanism connecting the two are unknown. IL-17A being a central pro-inflammatory cytokine in the pathogenesis of psoriasis may be involved in hepatic inflammation through its receptor and downward signaling; however so far no study has investigated IL-17A related signaling in the liver during psoriasis in a murine model. Therefore, this study explored psoriasis-induced hepatic inflammation and concurrent metabolic changes. Mice were applied topically imiquimod (IMQ) to develop psoriatic inflammation. Additionally mice were also treated either with IL-17A or anti-IL17A antibody to explore the role of IL-17 related signaling in liver. Mice were then assessed for hepatic inflammation through assessment of inflammatory/oxidative stress markers (IL-17RC, NFκB, IL-6, MCP-1, IL-1ß, GM-CSF, ICAM-1, iNOS, lipid peroxides and myeloperoxidase activity) as well as hepatic injury (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and protein/lipid metabolic biomarkers (total proteins, albumin, total bilirubin, triglycerides, HDL cholesterol, and total cholesterol). IMQ treatment led to hepatic inflammation as evidenced by increased pro-inflammatory cytokines and oxidative stress with concomitant dysregulation in hepatic protein/lipid metabolism. Treatment with IL-17A further aggravated, whereas treatment with anti-IL17A antibody ameliorated IMQ-induced changes in hepatic injury/inflammation and protein/lipid metabolism. Our study shows for the first time that psoriatic inflammation leads to hepatic inflammation which results in dysregulated protein/lipid metabolism through IL-17RC/NFκB signaling. This could result in increased risk of cardiovascular dysfunction in patients with psoriasis.
[Mh] Termos MeSH primário: Metabolismo Energético
Hepatite/etiologia
Hepatite/metabolismo
Interleucina-17/metabolismo
Psoríase/complicações
Receptores de Interleucina-17/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Citocinas/metabolismo
Modelos Animais de Doenças
Metabolismo dos Lipídeos
Peroxidação de Lipídeos
Masculino
Camundongos
NF-kappa B/metabolismo
Estresse Oxidativo
Peroxidase/metabolismo
Psoríase/imunologia
Psoríase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (Interleukin-17); 0 (NF-kappa B); 0 (Receptors, Interleukin-17); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  3 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28898718
[Au] Autor:Ganesan R; Rasool M
[Ad] Endereço:Immunopathology Lab, School of Bio Sciences and Technology, VIT University, Vellore 632 014, Tamilnadu, India.
[Ti] Título:Interleukin 17 regulates SHP-2 and IL-17RA/STAT-3 dependent Cyr61, IL-23 and GM-CSF expression and RANKL mediated osteoclastogenesis by fibroblast-like synoviocytes in rheumatoid arthritis.
[So] Source:Mol Immunol;91:134-144, 2017 11.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Interleukin (IL)-17 predominately produced by the Th17 cells, plays a crucial role in the fibroblast-like synoviocytes (FLS) mediated disease process of rheumatoid arthritis (RA). IL-17 exerts its pathogenic effects in RA-FLS by IL-17/IL-17RA/STAT-3 signaling. Recent studies have shown that RA-FLS produces SHP-2, Cyr61, IL-23, GM-CSF and RANKL which results in worsening of the disease. However, whether IL-17/IL-17RA/STAT-3 signaling regulates SHP-2, Cyr61, IL-23, GM-CSF and RANKL expressions in RA-FLS remains unknown. In this study, IL-17 treatment dramatically induced the production of Cyr61, IL-23 and GM-CSF in FLS isolated from adjuvant induced arthritis (AA) rats. Conversely, IL-17 mediated production of Cyr61, IL-23 and GM-CSF was abrogated by knockdown of IL-17RA using a small interfering RNA or blockade of STAT-3 activation with S3I-201 in AA-FLS. Interestingly, IL-17 treatment noticeably increased the expression of IL-17RA and SHP-2 in AA-FLS. However, silencing of IL-17RA reversed the effect of IL-17 on the expression of IL-17RA and SHP-2 in AA-FLS. In addition, an increased number of TRAP-positive multinucleated cells were observed in a coculture system consisting of IL-17 treated AA-FLS and rat bone marrow derived monocytes/macrophages. Further, mechanistically we found that IL-17 upregulated RANKL expression in AA-FLS that was dependent on the IL-17/IL-17RA/STAT-3 signaling cascade. Knockdown of IL-17RA or inhibition of STAT-3 activation decreased the IL- 17 induced RANKL expression by AA-FLS and their osteoclastogenic potential. Taken together, our findings demonstrate that IL-17 regulates SHP-2 expression and IL-17RA/STAT-3 dependent production of Cyr61, IL-23, GM-CSF and RANKL in AA-FLS and may reveal a new insight into the pathogenesis of RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Proteína Rica em Cisteína 61/imunologia
Fibroblastos/imunologia
Regulação da Expressão Gênica/imunologia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/imunologia
Interleucina-17/imunologia
Interleucina-23/imunologia
Osteoclastos/imunologia
Proteína Tirosina Fosfatase não Receptora Tipo 11/imunologia
Ligante RANK/imunologia
Receptores de Interleucina-17/imunologia
Fator de Transcrição STAT3/imunologia
Transdução de Sinais/imunologia
Membrana Sinovial/imunologia
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/patologia
Fibroblastos/patologia
Osteoclastos/patologia
Ratos
Ratos Wistar
Membrana Sinovial/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyr61 protein, rat); 0 (Cysteine-Rich Protein 61); 0 (Interleukin-17); 0 (Interleukin-23); 0 (RANK Ligand); 0 (Receptors, Interleukin-17); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, rat); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 11)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171120
[Lr] Data última revisão:
171120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE


  4 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28898280
[Au] Autor:Angkasekwinai P; Sodthawon W; Jeerawattanawart S; Hansakon A; Pattanapanyasat K; Wang YH
[Ad] Endereço:Department of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani Thailand.
[Ti] Título:ILC2s activated by IL-25 promote antigen-specific Th2 and Th9 functions that contribute to the control of Trichinella spiralis infection.
[So] Source:PLoS One;12(9):e0184684, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-25, an IL-17 family cytokine, derived from epithelial cells was shown to regulate Th2- and Th9-type immune responses. We previously reported that IL-25 was important in promoting efficient protective immunity against T. spiralis infection; however, the cellular targets of IL-25 to elicit type-2 immunity during infection have not yet been addressed. Here, we investigated IL-25-responding cells and their involvement in mediating type-2 immune response during T. spiralis infection. ILC2 and CD4+ Th2 cells residing in the gastrointestinal tract of T. spiralis infected mice were found to express high levels of surface interleukin-17 receptor B (IL-17RB), a component of the IL-25 receptor. Following T. spiralis infection, activated ILC2s upregulated surface MHCII expression and enhanced capacity of effector T helper cell in producing antigen-specific Th2 and Th9 cytokines through MHCII-dependent interactions. Reciprocally, lack of CD4+ T helper cells impaired ILC2 function to produce type 2-associated cytokines in responding to IL-25 during T. spiralis infection. Furthermore, mice deficient in IL-17RB showed markedly reduced ILC2 numbers and antigen-specific Th2 and Th9 cytokine production during T. spiralis infection. The Il17rb-/- mice failed to mount effective antigen specific Th2 and Th9 functions resulting in diminished goblet cell and mast cell responses, leading to delayed worm expulsion in the intestines and muscles. Thus, our data indicated that ILC2s and CD4+ Th2 cells are the predominant cellular targets of IL-25 following T. spiralis infection and their collaborative interactions may play a key role in mounting effective antigen-specific Th2 and Th9 cytokine responses against T. spiralis infection.
[Mh] Termos MeSH primário: Interleucina-17/metabolismo
Receptores de Interleucina-17/metabolismo
Células Th2/imunologia
Triquinelose/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Genes MHC Classe II
Células Caliciformes/imunologia
Imunidade Inata
Interleucina-10/metabolismo
Mastócitos/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Receptores de Interleucina-17/genética
Trichinella spiralis/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Il17rb protein, mouse); 0 (Il19 protein, mouse); 0 (Interleukin-17); 0 (Receptors, Interleukin-17); 130068-27-8 (Interleukin-10)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184684


  5 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28886140
[Au] Autor:Kwon YC; Kim JJ; Yun SW; Yu JJ; Yoon KL; Lee KY; Kil HR; Kim GB; Han MK; Song MS; Lee HD; Ha KS; Sohn S; Ebata R; Hamada H; Suzuki H; Ito K; Onouchi Y; Hong YM; Jang GY; Lee JK; Korean Kawasaki Disease Genetics Consortium
[Ad] Endereço:Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea.
[Ti] Título:Male-specific association of the FCGR2A His167Arg polymorphism with Kawasaki disease.
[So] Source:PLoS One;12(9):e0184248, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kawasaki disease (KD) is an acute systemic vasculitis that can potentially cause coronary artery aneurysms in some children. KD occurs approximately 1.5 times more frequently in males than in females. To identify sex-specific genetic variants that are involved in KD pathogenesis in children, we performed a sex-stratified genome-wide association study (GWAS), using the Illumina HumanOmni1-Quad BeadChip data (249 cases and 1,000 controls) and a replication study for the 34 sex-specific candidate SNPs in an independent sample set (671 cases and 3,553 controls). Male-specific associations were detected in three common variants: rs1801274 in FCGR2A [odds ratio (OR) = 1.40, P = 9.31 × 10-5], rs12516652 in SEMA6A (OR = 1.87, P = 3.12 × 10-4), and rs5771303 near IL17REL (OR = 1.57, P = 2.53 × 10-5). The male-specific association of FCGR2A, but not SEMA6A and IL17REL, was also replicated in a Japanese population (OR = 1.74, P = 1.04 × 10-4 in males vs. OR = 1.22, P = 0.191 in females). In a meta-analysis with 1,461 cases and 5,302 controls, a very strong association of KD with the nonsynonymous SNP rs1801274 (p.His167Arg, previously assigned as p.His131Arg) in FCGR2A was confirmed in males (OR = 1.48, P = 1.43 × 10-7), but not in the females (OR = 1.17, P = 0.055). The present study demonstrates that p.His167Arg, a KD-associated FCGR2A variant, acts as a susceptibility gene in males only. Overall, the gender differences associated with FCGR2A in KD provide a new insight into KD susceptibility.
[Mh] Termos MeSH primário: Substituição de Aminoácidos
Códon
Predisposição Genética para Doença
Síndrome de Linfonodos Mucocutâneos/genética
Polimorfismo de Nucleotídeo Único
Receptores de IgG/genética
[Mh] Termos MeSH secundário: Alelos
Grupo com Ancestrais do Continente Asiático/genética
Estudos de Casos e Controles
Feminino
Estudos de Associação Genética
Genótipo
Seres Humanos
Japão
Masculino
Razão de Chances
Receptores de Interleucina-17/genética
República da Coreia
Semaforinas/genética
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon); 0 (FCGR2A protein, human); 0 (IL17REL protein, human); 0 (Receptors, IgG); 0 (Receptors, Interleukin-17); 0 (SEMA6A protein, human); 0 (Semaphorins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184248


  6 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28771607
[Au] Autor:Park SK; Jin YD; Park YK; Yeon SH; Xu J; Han RN; Rha KS; Kim YM
[Ad] Endereço:Department of Otorhinolaryngology-Head and Neck Surgery, Research Institute for Medical Science, Chungnam National University School of Medicine, Daejeon, Korea.
[Ti] Título:IL-25-induced activation of nasal fibroblast and its association with the remodeling of chronic rhinosinusitis with nasal polyposis.
[So] Source:PLoS One;12(8):e0181806, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND OBJECTIVE: Interleukin (IL)-25 has been shown to play an important role in the pathogenesis of chronic rhinosinusitis with nasal polyps. Nasal polyps are associated with chronic inflammation of the mucous membranes in the paranasal sinuses and are involved in extracellular matrix (ECM) accumulation. The aim of this study is to evaluate the effects of IL-25 on myofibroblast differentiation, ECM production and the expression of matrix metalloproteinases in nasal polyp derived fibroblasts (NPDFs) and to determine the molecular mechanism underlying these processes. MATERIALS AND METHODS: A total of 40 patients were enrolled in this study for Immunofluorescence studies. Expression of IL17 receptor B was evaluated by real time reverse transcription polymerase chain reaction (PCR) in NPDFs. NPDFs were stimulated with IL-25 for 48 h in the presence or absence of mitogen-activated protein kinase (MAPK) and NF-κB inhibitors or small interfering RNAs (siRNA). The protein levels of fibrosis active mediators were examined using western blotting. Fibroblast migration was evaluated with a scratch assay. The total collagen amount was analyzed with the Sircol collagen assay. RESULTS: IL-25 induced α-SMA, fibronectin, and MMP-1 and -13, which were dependent on IL-17RB. IL-25 also induced activation of NF-κB and mitogen-activated protein kinase (MAPKs). By using the specific inhibitor of ERK, p38, JNK and NF-κB (U, SB, SP and Bay), we found that IL-25-induced expressions of α-SMA, fibronectin, and MMPs was regulated by the signaling pathways of MAPKs and NF-κB. IL-25 also induces α-SMA, fibronectin, and MMPs expression through IL-17RB-dependent pathways in NPDFs. The increased migration ability induced by IL-25 was suppressed by the specific inhibitors of MAPKs and NF-κB. CONCLUSION: Our data indicate that IL-25 induced myofibroblast differentiation, fibronectin production, and MMP-1 and -13 expressions through the signaling pathways of MAPKs and NF-κB. in NPDFs and increased expression of IL-25 were also involved in the pathogenesis of nasal polyposis by affecting nasal fibroblasts in chronic rhinosinusitis with nasal polyps.
[Mh] Termos MeSH primário: Fibroblastos/efeitos dos fármacos
Fibroblastos/patologia
Interleucina-17/farmacologia
Pólipos Nasais/complicações
Nariz/patologia
Sinusite/patologia
[Mh] Termos MeSH secundário: Actinas/metabolismo
Adulto
Diferenciação Celular/efeitos dos fármacos
Movimento Celular/efeitos dos fármacos
Ativação Enzimática/efeitos dos fármacos
Feminino
Fibronectinas/biossíntese
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Metaloproteinase 1 da Matriz/metabolismo
Metaloproteinase 13 da Matriz/metabolismo
Meia-Idade
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Receptores de Interleucina/genética
Receptores de Interleucina-17/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sinusite/genética
Sinusite/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Fibronectins); 0 (IL-25 receptor protein, human); 0 (Interleukin-17); 0 (NF-kappa B); 0 (Receptors, Interleukin); 0 (Receptors, Interleukin-17); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); EC 3.4.24.- (Matrix Metalloproteinase 13); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181806


  7 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28739823
[Au] Autor:Wang W; Liu W; Liu J; Wang Z; Fan F; Ma Y; Jin C; Xiang Y; Huang Y; Zhang X; Xu W; Yin Y; He Y
[Ad] Endereço:Department of Laboratory Medicine, Key Laboratory of Diagnostic Medicine (Ministry of Education), Chongqing Medical University, Chongqing, People's Republic of China.
[Ti] Título:Interleukin-17A Aggravates Middle Ear Injury Induced by Streptococcus pneumoniae through the p38 Mitogen-Activated Protein Kinase Signaling Pathway.
[So] Source:Infect Immun;85(10), 2017 Oct.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute otitis media (AOM) is one of the most common bacterial infectious diseases in children aged 2 to 7 years worldwide. We previously demonstrated that interleukin-17A (IL-17A) promotes an acute inflammatory response characterized by the influx of neutrophils into the middle ear cavity during -induced AOM. In general, the inflammatory response is viewed as an effector that frequently causes local tissue damage. However, little is known about the pathogenic effects of IL-17A in AOM. Here, we investigated the pathogenic effects of IL-17A by using wild-type (WT) and IL-17A knockout (KO) mouse models. The results showed that the pathogenic effects of AOM, including weight loss, histopathological changes, and proinflammatory cytokine production, were more severe in WT mice than in IL-17A KO mice, suggesting that IL-17A aggravates tissue damage in AOM. Furthermore, these pathogenic effects were found to be dependent on p38 mitogen-activated protein kinase (MAPK) and could be reversed in the presence of a p38 MAPK-specific inhibitor. It was also demonstrated that IL-17A promoted the production of neutrophil myeloperoxidase (MPO) through the p38 MAPK signaling pathway, which was responsible for the middle ear tissue injury. These data support the conclusion that IL-17A contributes to middle ear injury through the p38 MAPK signaling pathway.
[Mh] Termos MeSH primário: Orelha Média/patologia
Interleucina-17/imunologia
Sistema de Sinalização das MAP Quinases
Otite Média/patologia
Streptococcus pneumoniae/imunologia
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Orelha Média/imunologia
Orelha Média/microbiologia
Interleucina-17/deficiência
Interleucina-17/genética
Camundongos
Camundongos Knockout
Neutrófilos/imunologia
Otite Média/imunologia
Otite Média/metabolismo
Otite Média/microbiologia
Peroxidase/metabolismo
Receptores de Interleucina-17/metabolismo
Infecções Estreptocócicas/imunologia
Infecções Estreptocócicas/metabolismo
Infecções Estreptocócicas/microbiologia
Infecções Estreptocócicas/patologia
Streptococcus pneumoniae/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-17); 0 (Receptors, Interleukin-17); EC 1.11.1.7 (Peroxidase); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


  8 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28733485
[Au] Autor:Ghosh D; Brown SL; Stumhofer JS
[Ad] Endereço:Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.
[Ti] Título:IL-17 Promotes Differentiation of Splenic LSK Lymphoid Progenitors into B Cells following Infection.
[So] Source:J Immunol;199(5):1783-1795, 2017 Sep 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lineage Sca-1 c-Kit (LSK ) cells are a lymphoid progenitor population that expands in the spleen and preferentially differentiates into mature B cells in response to infection in mice. Furthermore, LSK derived B cells can subsequently contribute to the ongoing immune response through the generation of parasite-specific Ab-secreting cells, as well as germinal center and memory B cells. However, the factors that promote their differentiation into B cells in the spleen postinfection are not defined. In this article, we show that LSK cells produce the cytokine IL-17 in response to infection. Using mice, IL-17R signaling in cells other than LSK cells was found to support their differentiation into B cells. Moreover, primary splenic stromal cells grown in the presence of IL-17 enhanced the production of CXCL12, a chemokine associated with B cell development in the bone marrow, by a population of IL-17RA-expressing podoplanin CD31 stromal cells, a profile associated with fibroblastic reticular cells. Subsequent blockade of CXCL12 in vitro reduced differentiation of LSK cells into B cells, supporting a direct role for this chemokine in this process. Immunofluorescence indicated that podoplanin stromal cells in the red pulp were the primary producers of CXCL12 after infection. Furthermore, podoplanin staining on stromal cells was more diffuse, and CXCL12 staining was dramatically reduced in mice postinfection. Together, these results identify a distinct pathway that supports lymphoid development in the spleen during acute infection.
[Mh] Termos MeSH primário: Células Produtoras de Anticorpos/fisiologia
Linfócitos B/fisiologia
Interleucina-17/metabolismo
Células Progenitoras Linfoides/fisiologia
Malária/imunologia
Plasmodium yoelii/imunologia
Baço/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Antiprotozoários/metabolismo
Células Produtoras de Anticorpos/parasitologia
Linfócitos B/parasitologia
Diferenciação Celular
Células Cultivadas
Quimiocina CXCL12/metabolismo
Feminino
Seres Humanos
Memória Imunológica
Células Progenitoras Linfoides/parasitologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Proto-Oncogênicas pp60(c-src)/metabolismo
Receptores de Interleucina-17/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Protozoan); 0 (Chemokine CXCL12); 0 (Il17r protein, mouse); 0 (Interleukin-17); 0 (Receptors, Interleukin-17); EC 2.7.1.- (Matk protein, mouse); EC 2.7.10.2 (Proto-Oncogene Proteins pp60(c-src))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170723
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601972


  9 / 556 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28670688
[Au] Autor:Agnihotri P; Robertson NM; Umetsu SE; Arakcheeva K; Winandy S
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
[Ti] Título:Lack of Ikaros cripples expression of Foxo1 and its targets in naive T cells.
[So] Source:Immunology;152(3):494-506, 2017 Nov.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ikaros is a transcription factor that regulates lymphocyte development from the level of the haematopoietic stem cell. Lack of Ikaros reduces the ability of progenitor cells to commit to the T-cell lineage, resulting in reduced numbers of early thymic T-cell progenitors and mature T cells. Mature CD4 T cells that lack Ikaros have defects in proliferation, T helper cell differentiation, cytokine expression and the ability to become anergic. A role for Ikaros in the naive T cell has not yet been identified. The receptors interleukin-7 receptor α (IL-7Rα) and l-selectin are important for ensuring survival and proper homing of naive T cells, respectively. Here we show that lack of Ikaros leads to reduced expression of these receptors in naive T cells, which impacts their ability to home and survive in response to IL-7. We define the mechanism underlying this phenotype as a requirement for Ikaros in maintenance of expression of Foxo1, a transcriptional regulator that is required for their expression. We also demonstrate that CD4 T cells lacking Ikaros are significantly crippled in their ability to become induced regulatory T cells, a phenotype also linked to reduced Foxo1 expression. Finally, we show that restoring Ikaros function to Ikaros-deficient CD4 T cells increases levels of Foxo1 message. Together, these studies define, for the first time, a role for Ikaros in naive T cells and establish it as the first transcriptional regulator required for maintaining levels of Foxo1 gene expression in these cells.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/metabolismo
Proteína Forkhead Box O1/metabolismo
Fator de Transcrição Ikaros/deficiência
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/transplante
Diferenciação Celular
Sobrevivência Celular
Células Cultivadas
Quimiotaxia de Leucócito
Proteína Forkhead Box O1/genética
Proteína Forkhead Box O1/imunologia
Regulação da Expressão Gênica
Genótipo
Fator de Transcrição Ikaros/genética
Fator de Transcrição Ikaros/imunologia
Interleucina-7/farmacologia
Selectina L/genética
Selectina L/imunologia
Selectina L/metabolismo
Camundongos da Linhagem 129
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Receptores de Interleucina-17/genética
Receptores de Interleucina-17/imunologia
Receptores de Interleucina-17/metabolismo
Linfócitos T Reguladores/imunologia
Linfócitos T Reguladores/metabolismo
Fatores de Tempo
Transcrição Genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Il17r protein, mouse); 0 (Interleukin-7); 0 (Receptors, Interleukin-17); 0 (Zfpn1a1 protein, mouse); 126880-86-2 (L-Selectin); 148971-36-2 (Ikaros Transcription Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12786


  10 / 556 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28650001
[Au] Autor:Puig L
[Ad] Endereço:Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain. lpuig@santpau.cat.
[Ti] Título:Brodalumab: the first anti-IL-17 receptor agent for psoriasis.
[So] Source:Drugs Today (Barc);53(5):283-297, 2017 May.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Psoriasis is a chronic immune-mediated inflammatory skin disease in which the alteration of the interleukin-23 (IL-23)/IL-17 cytokine axis appears to be crucial from a pathogenetic perspective. This has been confirmed by the efficacy of monoclonal antibodies blocking IL-17A, such as secukinumab and ixekizumab. Brodalumab is a human anti-IL-17 receptor A (IL-17RA) monoclonal antibody that inhibits the biological activity of IL-17A, IL-17F and other IL-17 isoforms, and has been approved (210 mg s.c. at weeks 0, 1, 2 and every 2 weeks thereafter) for the treatment of psoriasis vulgaris, psoriatic arthritis, pustular psoriasis and psoriatic erythroderma in Japan (Lumicef). The U.S. Food and Drug Administration has also recently approved brodalumab (Siliq) for the treatment of moderate to severe plaque psoriasis in adult patients who are candidates for systemic therapy or phototherapy and have failed to respond or have lost response to other systemic therapies. Regulatory applications are under review in the E.U. and Canada. The phase III clinical trials in moderate to severe plaque psoriasis met their primary endpoints after 12 weeks' treatment, with PASI 75 (75% improvement in the Psoriasis Area and Severity Index) response rates ranging between 83% and 86% (210 mg) and PASI 100 response rates ranging between 37% and 44%, significantly higher than those achieved with ustekinumab in the head-to-head trials AMAGINE-1 and AMAGINE-2. The most frequently reported adverse events in brodalumab clinical trials consisted of nasopharyngitis, headache, upper respiratory tract infection and arthralgia. In the head-to-head trials, rates of neutropenia were higher with both active drugs than with placebo, and mild or moderate Candida infections were more frequent with brodalumab than with ustekinumab or placebo. Clinical development was terminated by Amgen after adverse events of suicidal ideation and behavior were observed ls involving several indications, but data are inconclusive regarding potential drug causality, and brodalumab has recently been approved in the U.S. with a black box warning and a risk-management program regarding suicidal issues. Blocking IL-17RA provides a highly efficacious therapeutic alternative for moderate to severe psoriasis with a satisfactory safety profile.
[Mh] Termos MeSH primário: Anti-Inflamatórios/uso terapêutico
Anticorpos Monoclonais/uso terapêutico
Psoríase/tratamento farmacológico
Receptores de Interleucina-17/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios/efeitos adversos
Anti-Inflamatórios/farmacocinética
Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/farmacocinética
Seres Humanos
Psoríase/diagnóstico
Psoríase/imunologia
Receptores de Interleucina-17/imunologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antibodies, Monoclonal); 0 (IL17RA protein, human); 0 (Receptors, Interleukin-17); 6ZA31Y954Z (brodalumab)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.5.2613690



página 1 de 56 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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