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[PMID]:28468967
[Au] Autor:Keller B; Stumpf I; Strohmeier V; Usadel S; Verhoeyen E; Eibel H; Warnatz K
[Ad] Endereço:Center for Chronic Immunodeficiency, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
[Ti] Título:High SYK Expression Drives Constitutive Activation of CD21 B Cells.
[So] Source:J Immunol;198(11):4285-4292, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human CD21 B cells present with an activated phenotype and accumulate in distinct disorders connected with chronic immune stimulation. Signaling studies had revealed an increased basal phosphorylation of spleen tyrosine kinase (SYK) and phospholipase Cγ2. Additional BCR stimulation of these constitutively active cells, however, led to reduced activation of these signaling molecules and subsequently NF-κB and Ca activation. In this article, we demonstrate that high SYK expression is a common feature of CD21 B cells independent of the underlying disorder, and that this high expression is sufficient to drive constitutive phosphorylation of SYK and its immediate targets Bruton's tyrosine kinase and phospholipase Cγ2. Inhibition of SYK activity eliminated features of the constitutive activation in these cells and partly restored BCR signaling. High SYK expression is especially induced by CpG or CD40L in combination with IL-21, but not BCR stimulation, suggesting the importance of the immune-stimulatory context for the induction of this B cell phenotype. In summary, high SYK expression is a common feature of human CD21 B cells and presumably results from chronic activation in inflammatory environments present in a subgroup of patients with heterogeneous disorders like chronic infection, autoimmunity, and immunodeficiency. High SYK expression by itself drives the constitutive activation observed in these B cells, which in turn may contribute to the hyporesponsiveness upon BCR stimulation. Given the high prevalence of autoreactive clones among CD21 B cells in autoimmune disorders, the dominant role of SYK in CD21 B cells may provide a new option for therapeutic interventions in patients with expanded CD21 B cells and humoral autoimmunity.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Ativação Linfocitária
Receptores de Complemento 3d/imunologia
Quinase Syk/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Linfócitos B/fisiologia
Ligante de CD40/imunologia
Feminino
Seres Humanos
Interleucinas/farmacologia
Masculino
Meia-Idade
Oligodesoxirribonucleotídeos/imunologia
Fosfolipase C gama/metabolismo
Fosforilação
Proteínas Tirosina Quinases/metabolismo
Receptores de Antígenos de Linfócitos B/imunologia
Transdução de Sinais
Quinase Syk/antagonistas & inibidores
Quinase Syk/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CPG-oligonucleotide); 0 (Interleukins); 0 (Oligodeoxyribonucleotides); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Complement 3d); 0 (interleukin-21); 147205-72-9 (CD40 Ligand); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (SYK protein, human); EC 2.7.10.2 (Syk Kinase); EC 3.1.4.3 (Phospholipase C gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700079


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[PMID]:28461568
[Au] Autor:Han W; Jackson DA; Matissek SJ; Misurelli JA; Neil MS; Sklavanitis B; Amarsaikhan N; Elsawa SF
[Ad] Endereço:Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115.
[Ti] Título:Novel Molecular Mechanism of Regulation of CD40 Ligand by the Transcription Factor GLI2.
[So] Source:J Immunol;198(11):4481-4489, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interaction between tumor cells and their surrounding microenvironment is essential for the growth and persistence of cancer cells. This interaction is mediated, in part, by cytokines. Although the role of cytokines in normal and malignant cell biology is well established, many of the molecular mechanisms regulating their expression remain elusive. In this article, we provide evidence of a novel pathway controlling the transcriptional activation of CD40L in bone marrow-derived stromal cells. Using a PCR-based screening of cytokines known to play a role in the biology of bone marrow malignancies, we identified CD40L as a novel GLI2 target gene in stromal cells. CD40L plays an important role in malignant B cell biology, and we found increased Erk phosphorylation and cell growth in malignant B cells cocultured with CD40L-expressing stromal cells. Further analysis indicated that GLI2 overexpression induced increased CD40L expression, and, conversely, GLI2 knockdown reduced CD40L expression. Using luciferase and chromatin immunoprecipitation assays, we demonstrate that GLI2 directly binds and regulates the activity of the CD40L promoter. We found that the CCR3-PI3K-AKT signaling modulates the GLI2-CD40L axis, and GLI2 is required for CCR3-PI3K-AKT-mediated regulation of the CD40L promoter. Finally, coculture of malignant B cells with cells stably expressing human CD40L results in increased Erk phosphorylation and increased malignant B cell growth, indicating that CD40L in the tumor microenvironment promotes malignant B cell activation. Therefore, our studies identify a novel molecular mechanism of regulation of CD40L by the transcription factor GLI2 in the tumor microenvironment downstream of CCR3 signaling.
[Mh] Termos MeSH primário: Ligante de CD40/genética
Fatores de Transcrição Kruppel-Like/metabolismo
Células Mesenquimais Estromais/imunologia
Células Mesenquimais Estromais/metabolismo
Proteínas Nucleares/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Linfócitos B/patologia
Ligante de CD40/imunologia
Ligante de CD40/metabolismo
Imunoprecipitação da Cromatina
Citocinas/imunologia
Regulação Neoplásica da Expressão Gênica
Fatores de Transcrição Kruppel-Like/genética
Sistema de Sinalização das MAP Quinases
Camundongos
Proteínas Nucleares/genética
Fosforilação
Reação em Cadeia da Polimerase
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores CCR3/metabolismo
Proteína Gli2 com Dedos de Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ccr3 protein, mouse); 0 (Cytokines); 0 (GLI2 protein, human); 0 (Gli2 protein, mouse); 0 (Kruppel-Like Transcription Factors); 0 (Nuclear Proteins); 0 (Receptors, CCR3); 0 (Zinc Finger Protein Gli2); 147205-72-9 (CD40 Ligand); EC 2.7.11.1 (Akt1 protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601490


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[PMID]:28455435
[Au] Autor:Guo Y; Walsh AM; Fearon U; Smith MD; Wechalekar MD; Yin X; Cole S; Orr C; McGarry T; Canavan M; Kelly S; Lin TA; Liu X; Proudman SM; Veale DJ; Pitzalis C; Nagpal S
[Ad] Endereço:Immunology, Janssen Research, Spring House, PA 19477; yguo49@its.jnj.com snagpal2@its.jnj.com.
[Ti] Título:CD40L-Dependent Pathway Is Active at Various Stages of Rheumatoid Arthritis Disease Progression.
[So] Source:J Immunol;198(11):4490-4501, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The inflammatory CD40-CD40L pathway is implicated in various autoimmune diseases, but the activity status of this pathway in various stages of rheumatoid arthritis (RA) progression is unknown. In this study, we used gene signatures of CD40L stimulation derived from human immature dendritic cells and naive B cells to assess the expression of CD40-downstream genes in synovial tissues from anti-citrullinated protein Ab-positive arthralgia, undifferentiated arthritis (UA), early RA, and established RA cohorts in comparison with healthy donors. Interestingly, the expression of and active full-length was increased in the disease tissues, whereas that of a dominant-negative isoform was decreased. Gene set variation analysis revealed that CD40L-responsive genes in immature dendritic cells and naive B cells were significantly enriched in synovial tissues from UA, early RA, and established RA patients. Additionally, CD40L-induced naive B cell genes were also significantly enriched in synovial tissues from arthralgia patients. In our efforts to characterize downstream mediators of CD40L signaling, we have identified and as novel components of the pathway. In conclusion, our data suggest that therapeutic CD40-CD40L blocking agents may prove efficacious not only in early and established RA, but also in inhibiting the progression of the disease from arthralgia or UA to RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/imunologia
Artrite/imunologia
Ligante de CD40/imunologia
Ligante de CD40/metabolismo
Progressão da Doença
Transdução de Sinais
[Mh] Termos MeSH secundário: Adulto
Idoso
Artralgia/imunologia
Artralgia/fisiopatologia
Artrite Reumatoide/fisiopatologia
Linfócitos B/efeitos dos fármacos
Linfócitos B/imunologia
Biópsia
Linfócitos T CD4-Positivos/imunologia
Antígenos CD40/deficiência
Antígenos CD40/genética
Antígenos CD40/imunologia
Antígenos CD40/metabolismo
Ligante de CD40/genética
Ligante de CD40/farmacologia
Células Dendríticas/imunologia
Células Dendríticas/fisiologia
Feminino
Voluntários Saudáveis
Seres Humanos
Ativação Linfocitária
Masculino
Meia-Idade
Líquido Sinovial/citologia
Líquido Sinovial/imunologia
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD40 Antigens); 147205-72-9 (CD40 Ligand)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601988


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[PMID]:29183724
[Au] Autor:Seigner J; Basilio J; Resch U; de Martin R
[Ad] Endereço:Department of Vascular Biology and Thrombosis Research, Medical University of Vienna, A-1090 Vienna, Austria.
[Ti] Título:CD40L and TNF both activate the classical NF-κB pathway, which is not required for the CD40L induced alternative pathway in endothelial cells.
[So] Source:Biochem Biophys Res Commun;495(1):1389-1394, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD40L and TNF signal through engagement of their respective receptors, which are both members of the TNF receptor family. They use partially common signaling molecules leading, among others, to activation of the NF-κB pathway. However, whereas TNF activates the classical, CD40L has been reported to activate the alternative NF-κB pathway, leading to the anticipation that differences in the pattern of inflammatory gene expression would occur. Here, we have compared the gene expression repertoire of CD40L (CD154) and TNF stimulated HUVEC and report that unexpectedly, apart from a stronger response to TNF, no major qualitative differences could be observed. This applies for the period of up to 6 h, a time where the alternative pathway has already been activated. Analysis of the early events after receptor engagement revealed that both TNF and CD40L activate the classical NF-κB pathway, and confirm activation of the alternative by the latter. Furthermore, using genetic and pharmacological inhibition of the classical pathway we show that activation of the alternative occurs independently of the former. This reveals novel insights into NF-κB signaling by CD40L and TNF in endothelial cells.
[Mh] Termos MeSH primário: Ligante de CD40/imunologia
Células Endoteliais/imunologia
Regulação da Expressão Gênica/imunologia
Redes e Vias Metabólicas/imunologia
NF-kappa B/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Células Cultivadas
Seres Humanos
Transdução de Sinais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NF-kappa B); 0 (TNF protein, human); 0 (Tumor Necrosis Factor-alpha); 147205-72-9 (CD40 Ligand)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:28974444
[Au] Autor:Shi Y; Halperin SA; Lee SF
[Ad] Endereço:Department of Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada; Canadian Center for Vaccinology, Dalhousie University, Nova Scotia Health Authority, Izaak Walton Killam Health Centre, Halifax, Nova Scotia B3K 6R8, Canada.
[Ti] Título:Expression, purification, and functional analysis of an antigen-targeting fusion protein composed of CD40 ligand and the C-terminal fragment of ovalbumin.
[So] Source:Protein Expr Purif;142:37-44, 2018 Feb.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Delivering antigen via molecules specifically targeting receptors on the surface of antigen-presenting cells is a strategy to improve immune responses. In this study, an antigen-targeting fusion protein (OVA-CD40LS) composed of the C-terminal fragment of ovalbumin and the extracellular domain of mouse CD40 ligand was constructed by genetic fusion. The OVA-CD40LS and the control OVA (rOVA) genes were cloned in Escherichia coli and over-expressed as insoluble proteins. The rOVA protein was purified from the insoluble fraction of E. coli cell lysate by nickel affinity chromatography and refolded by step-wise dialysis to give a yield of 11.8 mg/L of culture. The OVA-CD40LS was purified by a 'two-round' nickel affinity and on-column protein-refolding chromatography. The yield was 528 µg/L of culture. The purified OVA-CD40LS, but not the rOVA, was able to simulate the production of pro-inflammatory cytokines and up-regulate cell surface marker proteins in mouse bone marrow-derived dendritic cells. The purified OVA-CD40LS elicited a robust immune response when injected submucosally in the oral cavity of mice. Collectively, the results indicate that the OVA-CD40LS fusion protein was biologically active, functioning as an antigen-targeting protein.
[Mh] Termos MeSH primário: Ligante de CD40/imunologia
Células Dendríticas/efeitos dos fármacos
Imunidade nas Mucosas/efeitos dos fármacos
Ovalbumina/imunologia
Plasmídeos/química
Proteínas Recombinantes de Fusão/biossíntese
[Mh] Termos MeSH secundário: Animais
Anticorpos/sangue
Células da Medula Óssea/citologia
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Ligante de CD40/genética
Clonagem Molecular
Células Dendríticas/citologia
Células Dendríticas/imunologia
Escherichia coli/genética
Escherichia coli/metabolismo
Feminino
Expressão Gênica
Imunização
Interleucina-6/biossíntese
Camundongos
Camundongos Endogâmicos BALB C
Mucosa Bucal/citologia
Mucosa Bucal/efeitos dos fármacos
Mucosa Bucal/imunologia
Ovalbumina/genética
Plasmídeos/metabolismo
Cultura Primária de Células
Proteínas Recombinantes de Fusão/administração & dosagem
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/imunologia
Fator de Necrose Tumoral alfa/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Interleukin-6); 0 (Recombinant Fusion Proteins); 0 (Tumor Necrosis Factor-alpha); 0 (interleukin-6, mouse); 147205-72-9 (CD40 Ligand); 9006-59-1 (Ovalbumin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE


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[PMID]:29023539
[Au] Autor:Gardell JL; Parker DC
[Ad] Endereço:Department of Molecular Microbiology and Immunology, Oregon Health & Science University, Portland, Oregon, United States of America.
[Ti] Título:Despite disorganized synapse structure, Th2 cells maintain directional delivery of CD40L to antigen-presenting B cells.
[So] Source:PLoS One;12(10):e0186573, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Upon recognition of peptide displayed on MHC molecules, Th1 and Th2 cells form distinct immunological synapse structures. Th1 cells have a bull's eye synapse structure with TCR/ MHC-peptide interactions occurring central to a ring of adhesion molecules, while Th2 cells have a multifocal synapse with small clusters of TCR/MHC interactions throughout the area of T cell/antigen-presenting cell interaction. In this study, we investigated whether this structural difference in the immunological synapse affects delivery of T cell help. The immunological synapse is thought to ensure antigen-specific delivery of cytolytic granules and killing of target cells by NK cells and cytolytic T cells. In helper T cells, it has been proposed that the immunological synapse may direct delivery of other effector molecules including cytokines. CD40 ligand (CD40L) is a membrane-bound cytokine essential for antigen-specific T cell help for B cells in the antibody response. We incubated Th1 and Th2 cells overnight with a mixture of antigen-presenting and bystander B cells, and the delivery of CD40L to B cells and subsequent B cell responses were compared. Despite distinct immunological synapse structures, Th1 and Th2 cell do not differ in their ability to deliver CD40L and T cell help in an antigen-specific fashion, or in their susceptibility to inhibition of help by a blocking anti-CD40L antibody.
[Mh] Termos MeSH primário: Células Apresentadoras de Antígenos/metabolismo
Linfócitos B/metabolismo
Ligante de CD40/metabolismo
Sinapses/química
Células Th2/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos/imunologia
Anticorpos/farmacologia
Células Apresentadoras de Antígenos/citologia
Linfócitos B/imunologia
Antígenos CD40/deficiência
Antígenos CD40/genética
Ligante de CD40/genética
Ligante de CD40/imunologia
Ciclosporina/farmacologia
Feminino
Sinapses Imunológicas/química
Sinapses Imunológicas/efeitos dos fármacos
Sinapses Imunológicas/imunologia
Interleucina-4/imunologia
Ativação Linfocitária/efeitos dos fármacos
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Microscopia Confocal
Sinapses/metabolismo
Células Th1/citologia
Células Th1/metabolismo
Células Th2/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD40 Antigens); 147205-72-9 (CD40 Ligand); 207137-56-2 (Interleukin-4); 83HN0GTJ6D (Cyclosporine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186573


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[PMID]:28964662
[Au] Autor:Desideri G; Bocale R; D'Amore A; Necozione S; Boscherini M; Carnassale G; Barini A; Barini A; Bellantone R; Lombardi CP
[Ad] Endereço:Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy. Electronic address: giovambattista.desideri@univaq.it.
[Ti] Título:Replacement therapy with levothyroxine modulates platelet activation in recent-onset post-thyroidectomy subclinical hypothyroidism.
[So] Source:Nutr Metab Cardiovasc Dis;27(10):896-901, 2017 Oct.
[Is] ISSN:1590-3729
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIM: Subclinical hypothyroidism has been linked to increased risk of atherosclerotic disease. Soluble CD40 ligand (sCD40L), mainly derived from activated platelets, and the lipid peroxidation product 8-iso-prostaglandin F (8-iso-PGF ) are known to play a relevant pathophysiological role in atherogenesis. In this study, we analyzed the relationship between thyroid hormones and circulating levels of sCD40L and 8-iso-PGF in patient with recent-onset post-thyroidectomy subclinical hypothyroidism under replacement therapy. METHODS AND RESULTS: Circulating levels of thyroid hormones, sCD40L, and 8-iso-PGF were assessed in 40 recently thyroidectomized patients (33 females, mean age 52.0 ± 11.7 years) at baseline (5-7 day after surgery) and after 2 months under replacement therapy with levothyroxine (LT-4). At baseline, circulating levels of thyroid hormones were indicative of a subclinical hypothyroidism (TSH 7.7 ± 3.9 µU/mL, FT3 1.8 ± 0.6 pg/mL, and FT3 8.9 ± 3.0 pg/mL). Circulating levels of sCD40L and 8-iso-PGF were directly correlated with each other (r = 0.360, p = 0.023) and with TSH levels (r = 0.322, p = 0.043 and r = 0.329 p = 0.038, respectively). After 2 months under the replacement therapy with LT-4 circulating levels of TSH (from 7.7 ± 3.9 to 2.7 ± 2.8 µU/mL, p < 0.0001), sCD40L (from 6.11 ± 2.41 to 2.43 ± 2.00 ng/mL, p < 0.0001) and 8-iso-PGF (from 45.33 ± 6.94 to 40.36 ± 6.20, p < 0.0001) significantly decreased. Changes in circulating levels of sCD40L and 8-iso-PGF were directly correlated with each other (r = 0.349 p = 0.028) and with changes in TSH levels (r = 0.367 p = 0.020 and r = 0.339 p = 0.032, respectively). CONCLUSION: Our study suggests an influential role of TSH on proatherogenic activation of platelets, probably through enhanced lipid peroxidation. These findings could partially explain the increased susceptibility of patients with subclinical hypothyroidism to develop atherosclerotic disease.
[Mh] Termos MeSH primário: Plaquetas/efeitos dos fármacos
Terapia de Reposição Hormonal
Hipotireoidismo/tratamento farmacológico
Ativação Plaquetária/efeitos dos fármacos
Tireoidectomia/efeitos adversos
Tiroxina/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Doenças Assintomáticas
Biomarcadores/sangue
Plaquetas/metabolismo
Ligante de CD40/sangue
Dinoprosta/análogos & derivados
Dinoprosta/sangue
Feminino
Seres Humanos
Hipotireoidismo/sangue
Hipotireoidismo/diagnóstico
Hipotireoidismo/etiologia
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Meia-Idade
Tireotropina/sangue
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Biomarkers); 147205-72-9 (CD40 Ligand); 27415-26-5 (8-epi-prostaglandin F2alpha); 9002-71-5 (Thyrotropin); B7IN85G1HY (Dinoprost); Q51BO43MG4 (Thyroxine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


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[PMID]:28877992
[Au] Autor:Salio M; Gasser O; Gonzalez-Lopez C; Martens A; Veerapen N; Gileadi U; Verter JG; Napolitani G; Anderson R; Painter G; Besra GS; Hermans IF; Cerundolo V
[Ad] Endereço:Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, United Kingdom; mariolina.salio@imm.ox.ac.uk.
[Ti] Título:Activation of Human Mucosal-Associated Invariant T Cells Induces CD40L-Dependent Maturation of Monocyte-Derived and Primary Dendritic Cells.
[So] Source:J Immunol;199(8):2631-2638, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mucosal-associated invariant T (MAIT) cells are innate T cells that recognize intermediates of the vitamin B2 biosynthetic pathway presented by the monomorphic MR1 molecule. It remains unclear whether, in addition to their cytolytic activity that is important in antimicrobial defense, MAIT cells have immune-modulatory functions that could enhance dendritic cell (DC) maturation. In this study, we investigated the molecular mechanisms dictating the interactions between human MAIT cells and DCs and demonstrate that human MAIT cells mature monocyte-derived and primary DCs in an MR1- and CD40L-dependent manner. Furthermore, we show that MAIT cell-derived signals synergize with microbial stimuli to induce secretion of bioactive IL-12 by DCs. Activation of human MAIT cells in whole blood leads to MR1- and cytokine-dependent NK cell transactivation. Our results underscore an important property of MAIT cells, which can be of translational relevance to rapidly orchestrate adaptive immunity through DC maturation.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Ativação Linfocitária
Células T Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Ligante de CD40/metabolismo
Comunicação Celular
Diferenciação Celular
Células Cultivadas
Antígenos de Histocompatibilidade Classe I/metabolismo
Seres Humanos
Imunidade nas Mucosas
Interleucina-12/metabolismo
Antígenos de Histocompatibilidade Menor/metabolismo
Monócitos/imunologia
Receptor Cross-Talk
Riboflavina/imunologia
Riboflavina/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I); 0 (MR1 protein, human); 0 (Minor Histocompatibility Antigens); 147205-72-9 (CD40 Ligand); 187348-17-0 (Interleukin-12); TLM2976OFR (Riboflavin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700615


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[PMID]:28848067
[Au] Autor:Nakayama Y; Kosek J; Capone L; Hur EM; Schafer PH; Ringheim GE
[Ad] Endereço:Inflammation and Immunology Translational Development, Celgene Corporation, Summit, NJ 07901.
[Ti] Título:Aiolos Overexpression in Systemic Lupus Erythematosus B Cell Subtypes and BAFF-Induced Memory B Cell Differentiation Are Reduced by CC-220 Modulation of Cereblon Activity.
[So] Source:J Immunol;199(7):2388-2407, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BAFF is a B cell survival and maturation factor implicated in the pathogenesis of systemic lupus erythematosus (SLE). In this in vitro study, we describe that soluble BAFF in combination with IL-2 and IL-21 is a T cell contact-independent inducer of human B cell proliferation, plasmablast differentiation, and IgG secretion from circulating CD27 memory and memory-like CD27 IgD double-negative (DN) B cells, but not CD27 IgD naive B cells. In contrast, soluble CD40L in combination with IL-2 and IL-21 induces these activities in both memory and naive B cells. Blood from healthy donors and SLE patients have similar circulating levels of IL-2, whereas SLE patients exhibit elevated BAFF and DN B cells and reduced IL-21. B cell differentiation transcription factors in memory, DN, and naive B cells in SLE show elevated levels of Aiolos, whereas Ikaros levels are unchanged. Treatment with CC-220, a modulator of the cullin ring ligase 4-cereblon E3 ubiquitin ligase complex, reduces Aiolos and Ikaros protein levels and BAFF- and CD40L-induced proliferation, plasmablast differentiation, and IgG secretion. The observation that the soluble factors BAFF, IL-2, and IL-21 induce memory and DN B cell activation and differentiation has implications for extrafollicular plasmablast development within inflamed tissue. Inhibition of B cell plasmablast differentiation by reduction of Aiolos and Ikaros may have utility in the treatment of SLE, where elevated levels of BAFF and Aiolos may prime CD27 memory and DN memory-like B cells to become Ab-producing plasmablasts in the presence of BAFF and proinflammatory cytokines.
[Mh] Termos MeSH primário: Fator Ativador de Células B/sangue
Fator Ativador de Células B/imunologia
Subpopulações de Linfócitos B/imunologia
Fator de Transcrição Ikaros/genética
Memória Imunológica
Lúpus Eritematoso Sistêmico/imunologia
Peptídeo Hidrolases/metabolismo
[Mh] Termos MeSH secundário: Formação de Anticorpos/efeitos dos fármacos
Fator Ativador de Células B/metabolismo
Subpopulações de Linfócitos B/efeitos dos fármacos
Ligante de CD40/farmacologia
Diferenciação Celular
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Seres Humanos
Fator de Transcrição Ikaros/sangue
Memória Imunológica/efeitos dos fármacos
Interleucina-2/sangue
Interleucina-2/farmacologia
Interleucinas/farmacologia
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/deficiência
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B-Cell Activating Factor); 0 (CC-220); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (IKZF1 protein, human); 0 (IKZF3 protein, human); 0 (Interleukin-2); 0 (Interleukins); 0 (TNFSF13B protein, human); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (interleukin-21); 147205-72-9 (CD40 Ligand); 148971-36-2 (Ikaros Transcription Factor); EC 3.4.- (CRBN protein, human); EC 3.4.- (Peptide Hydrolases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601725


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[PMID]:28837666
[Au] Autor:Tung CH; Lu MC; Lai NS; Wu SF
[Ad] Endereço:Division of Allergy, Immunology and Rheumatology; Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Dalin, Chiayi, Taiwan, Republic of China.
[Ti] Título:Tumor necrosis factor-α blockade treatment decreased CD154 (CD40-ligand) expression in rheumatoid arthritis.
[So] Source:PLoS One;12(8):e0183726, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXTS: CD154 (commonly referred to as CD40-ligand) is a critical T cell factor that participates in the pathogenesis of autoimmune and is over-expressed in rheumatoid arthritis (RA). TNF-α blockade treatment had dramatic efficacy in RA. OBJECTIVE: To investigate whether TNF-α blockade treatment can inhibit CD154 expression in RA. METHODS: Blood samples were collected from 33 patients with rheumatoid arthritis before and 3 months after TNF-α blockade treatment. Clinical serological data determined by standard assays and T cell CD154 expression levels determined by flow cytometry were statistically analyzed for these two time points. RESULTS: The percentage of CD154 expression on gated CD4+ T cells of PBMCs from RA patients after 3 months TNF-α blockade treatment was significantly lower than before treatment (2.94 ± 3.21% vs. 7.21 ± 5.64%; p = 0.0001). The disease activity and anti-CCP antibody levels were also significantly reduced after TNF-α blockade treatment. The CD154 expression levels were positively correlated with disease activity index DAS28, and CRP. The post-stimulated CD154 expression percentage of purified CD4+ T cells between baseline and after TNF-α blockade treatment was not significantly different (p = 0.221). Baseline CD154 levels were positively correlated with treatment-induced changes in DAS28 (p = 0.014; r2 = 0.187). CONCLUSIONS: TNF-α blockade treatment significantly decreased the CD154 expression on CD4+ T cells, disease activity and anti-CCP antibody simultaneously in RA patients. However TNF-α blockade did not impair T cell capacity to express CD154 after stimulation. These results suggest that decreased CD154 expression after TNF-α blockade may be due to decreased RA disease activity but not direct inhibition of CD154 responsiveness of T cells.
[Mh] Termos MeSH primário: Artrite Reumatoide/tratamento farmacológico
Ligante de CD40/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
Artrite Reumatoide/metabolismo
Linfócitos T CD4-Positivos/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Necrosis Factor-alpha); 147205-72-9 (CD40 Ligand)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170825
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183726



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