Bibliografie tematiche / IL-10

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Letteratura scientifica selezionata sul tema "IL-10"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 11 marzo 2023

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Articoli di riviste sul tema "IL-10"

1

Commins, Scott, John W. Steinke e Larry Borish. "The extended IL-10 superfamily: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28, and IL-29". Journal of Allergy and Clinical Immunology 121, n. 5 (maggio 2008): 1108–11. http://dx.doi.org/10.1016/j.jaci.2008.02.026.

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Glocker, Erik-Oliver, Daniel Kotlarz, Christoph Klein, Neil Shah e Bodo Grimbacher. "IL-10 and IL-10 receptor defects in humans". Annals of the New York Academy of Sciences 1246, n. 1 (dicembre 2011): 102–7. http://dx.doi.org/10.1111/j.1749-6632.2011.06339.x.

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3

Wang, Min, Youji Hu, Ischiro Shima e Mark E. Stearns. "IL-10/IL-10 Receptor Signaling Regulates TIMP-1 Expression". Cancer Biology & Therapy 1, n. 5 (13 settembre 2002): 556–63. http://dx.doi.org/10.4161/cbt.1.5.222.

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4

Rennick, Donna M., e Madeline M. Fort. "XII. IL-10-deficient (IL-10−/−) mice and intestinal inflammation". American Journal of Physiology-Gastrointestinal and Liver Physiology 278, n. 6 (1 giugno 2000): G829—G833. http://dx.doi.org/10.1152/ajpgi.2000.278.6.g829.

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Abstract (sommario):
Interleukin (IL)-10−/−mice spontaneously develop intestinal inflammation characterized by discontinuous transmural lesions affecting the small and large intestine and by dysregulated production of proinflammatory cytokines. The uncontrolled generation of IFN-γ-producing CD4+T cells (Th1 type) has been shown to play a causal role in the development of enterocolitis affecting these mutants. This article discusses studies of IL-10−/−mice that have investigated the role of enteric organisms in triggering intestinal disease, the mediators responsible for initiating and maintaining intestinal disease, the role IL-10 plays in the generation and/or function of regulatory cells, and the results of IL-10 therapy in experimental animal models of inflammatory bowel disease (IBD) and human patients with IBD.
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5

Jankovic, Dragana, e Giorgio Trinchieri. "IL-10 or not IL-10: that is the question". Nature Immunology 8, n. 12 (dicembre 2007): 1281–83. http://dx.doi.org/10.1038/ni1207-1281.

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6

Mittal, Sharad K., Kyung-Jin Cho, Satoshi Ishido e Paul A. Roche. "Interleukin 10 (IL-10)-mediated Immunosuppression". Journal of Biological Chemistry 290, n. 45 (25 settembre 2015): 27158–67. http://dx.doi.org/10.1074/jbc.m115.682708.

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7

Ouyang, Wenjun, e Anne O’Garra. "IL-10 Family Cytokines IL-10 and IL-22: from Basic Science to Clinical Translation". Immunity 50, n. 4 (aprile 2019): 871–91. http://dx.doi.org/10.1016/j.immuni.2019.03.020.

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8

Conti, P., D. Kempuraj, S. Frydas, K. Kandere, W. Boucher, R. Letourneau, B. Madhappan, K. Sagimoto, S. Christodoulou e T. C. Theoharides. "IL-10 subfamily members: IL-19, IL-20, IL-22, IL-24 and IL-26". Immunology Letters 88, n. 3 (settembre 2003): 171–74. http://dx.doi.org/10.1016/s0165-2478(03)00087-7.

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9

Mahmood Majeed, Hameed, e Malik Hadi Qadurie. "Evaluation Relationship between IL-10, IL-1α in Hepatocellular Carcinoma Patients". Diyala Journal For Pure Science 13, n. 3 (1 luglio 2017): 103–12. http://dx.doi.org/10.24237/djps.1303.252b.

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10

Murray, Henry W., Christina M. Lu, Smita Mauze, Sherry Freeman, Andre L. Moreira, Gilla Kaplan e Robert L. Coffman. "Interleukin-10 (IL-10) in Experimental Visceral Leishmaniasis and IL-10 Receptor Blockade as Immunotherapy". Infection and Immunity 70, n. 11 (novembre 2002): 6284–93. http://dx.doi.org/10.1128/iai.70.11.6284-6293.2002.

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Abstract (sommario):
ABSTRACT Interleukin-10 (IL-10) is thought to promote intracellular infection, including human visceral leishmaniasis, by disabling Th1 cell-type responses and/or deactivating parasitized tissue macrophages. To develop a rationale for IL-10 inhibition as treatment in visceral infection, Th1 cytokine-driven responses were characterized in Leishmania donovani-infected BALB/c mice in which IL-10 was absent or overexpressed or its receptor (IL-10R) was blockaded. IL-10 knockout and normal mice treated prophylactically with anti-IL-10R demonstrated accelerated granuloma assembly and rapid parasite killing without untoward tissue inflammation; IL-12 and gamma interferon mRNA expression, inducible nitric oxide synthase reactivity, and responsiveness to antimony chemotherapy were also enhanced in knockout mice. In IL-10 transgenic mice, parasite replication was unrestrained, and except for antimony responsiveness, measured Th1 cell-dependent events were all initially impaired. Despite subsequent granuloma assembly, high-level infection persisted, and antimony-treated transgenic mice also relapsed. In normal mice with established infection, anti-IL-10R treatment was remarkably active, inducing near-cure by itself and synergism with antimony. IL-10's deactivating effects regulate outcome in experimental visceral leishmaniasis, and IL-10R blockade represents a potential immuno- and/or immunochemotherapeutic approach in this infection.
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Più fonti

Tesi sul tema "IL-10"

1

Frisch, Kristina. "Klonierung von IL-10 und IL-10-Homologen und Funktionsanalyse in einem Mausmodell der polymikrobiellen Sepsis". [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973392185.

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2

Ng, Tien Haeng Sky. "Mechanisms of IL-10 transcriptional regulation". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.702135.

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Previous work has shown that subcutaneous (s.c) specific immunotherapy (SIT) using the myelin protein peptide MBP Acl-9 [4Y] induces protection against EAE in the TCR transgenic Tg4 mice. Repeated administration of MBP Ac1-9 [4Y] was found to induce IL-1O expressing TH1 like cells which were termed IL-l0 Tregs. To further the understanding of how IL-1O transcription is regulated, the expression of IFN-y, IL-4, IL-1O, c-Maf, NFIL3 protein and mRNA, Gata3 mRNA and epigenetic modifications at the Il10 promoter were characterised for each dose of s.c MBP Ac 1-9 [4 Y] administration. The analysis revealed that c-Maf and NFIL3 positively correlated with Il-IO expression, whilst levels of H3K27me3 at the Il10 promoter, an epigenetic mark associated with transcriptional repression, correlated inversely with IL-IO expression. To investigate the therapeutic potential of non-antigen specific immunoregulatory small molecules, GSK3 inhibitors were co-cultured with murine TH1, TH2 and human memory T cells. The analysis shows that GSK3 inhibitors also induce IL-10 expression via transcriptional mechanisms in both murine Th cells and human memory T cells. Similar to IL-l0 Tregs, murine TH1 GSK3 inhibitor treated cells expressed higher levels of NFIL3 and c-Maf whilst murine TH2 GSK3 inhibitor treated cells expressed higher levels of NFIL3 only. In contrast to IL-10 Tregs both THI and TH2 cells expressed higher levels of Gata3 in response to GSK3 inhibitor treatment. In addition, epigenetic changes also take place in the Il10 promoter of GSK3 inhibitor treated murine TH1 and human memory T cells. Collectively these results show that it is possible to alter epigenetic modifications and induce IL-1O expression in murine TH1 and TH1-like cells with in vivo and in vitro methods. Furthermore, we propose combining the antigen specific s.c SIT with GSK3 inhibitors to improve the efficacy and safety of both treatments.
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Cordeiro, Cynthia Azeredo. "Polimorfismos dos Genes das Citocinas IL-1alfa, IL -1beta, IL-10 e TNF-alfa". Universidade Federal de Minas Gerais, 2008. http://hdl.handle.net/1843/RRSA-7F5KG7.

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Purpose: Toxoplasmic Retinochoroiditis (TR) is the most common identifiable cause of posterior uveitis in many parts of the world. There is a great controversy regarding which factors are responsible for the occurrence or reccurrence of TR. Experimental data have demonstrated a relevant role for IL-10, TNF-alfa, IL-1alfa and IL-1alfa in the modulation of acute ocular toxoplasmosis. Therefore, we aim to investigate thepossible association between an IL10 (-1082G/A), TNF-alfa (-308G/A), IL1A (-889C/T) and IL1B (+3954C/T) gene polymorphisms and TR in humans. Methods: One hundred patients with diagnosed TR were recruited from the Uveitis Section, Federal University of Minas Gerais. For comparison, one hundred healthy blood donors with positive serology for Toxoplasmosis and without retinal signs of previous TR were included in the study. Genomic DNA was obtained from oral swabs of individualsand amplified using polymerase chain reaction (PCR) with specific primers for each locus gene. PCR products were submitted to restriction endonuclease digestion and analyzed by polyacrylamide gel electrophoresis to distinguish specific alleles for eachgene, allowing the detection of the polymorphism and determination of genotypes.Results: In the IL10 gene polymorphism analysis, there was a significant difference in the genotype distribution between TR patients and control subjects (x² = 6.33, P = 0.04). Carriers of the IL10 -1082 A allele (AA + AG genotypes) were more often patients with TR than controls (x² = 5.97, P = 0.01, OR = 2.55, CI = 1.11Objetivos: A Retinocoroidite Toxoplasmica (RT) e a causa mais comum de uveite posterior em muitas partes do mundo, incluindo o Brasil. Existem grandes controversias com relacao aos fatores responsaveis pela ocorrencia ou recorrencia da RT. Dados experimentais demonstraram papel relevante da interleucina-10 (IL-10), fator de necrose tumoral (TNF-alfa), interleucina-1alfa (IL-1alfa) e interleucina-beta (IL-1beta) na modulacao da TO. A partir disso, foi proposto investigar a possivel associacao entre o polimorfismo funcional do gene IL10 na posicao .1082 (G/A), TNF-alfa na posicao .308 (G/A), IL1A na posicao .889 (C/T) e IL1B na posicao +3954 (C/T) e a RT em humanos. Metodologia: Cem pacientes com diagnostico de TO foram recrutados do Setor de Uveites da UFMG. Como controles, cem doadores de sangue com sorologia positiva para Toxoplasmose e sem historia e/ou sinais de TO previa foram incluidos no estudo. DNA foi obtido atraves do raspado de mucosa oral dos individuos e submetido a determinacao dos genotipos. Os fragmentos especificos de DNA foram amplificados pela reacao em cadeia da polimerase (PCR). Os produtos da PCR foram clivados por enzima de restricao e visualizados atraves de eletroforese para distinguir os alelos especificos de cada gene, permitindo a detecção do polimorfismo e determinacao dos genotipos. Resultados: Na analise do polimorfismo do gene IL10 (-1082G/A) foi encontrada diferenca significativa na distribuicao do genotipo entre pacientes e controles (x² = 6.33, P = 0.04). Carreadores do alelo IL10 -1082 A (genotipos AA + AG) foram mais frequentes entre pacientes do que entre os controles (x² = 5.97, P = 0.01, OR = 2.55, CI=1.11
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4

Wong, Li-Chuen. "IL-10 promoter polymorphisms in atopic dermatitis". Thesis, The University of Sydney, 2002. https://hdl.handle.net/2123/27849.

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Atopic dermatitis (AD) is one of the many clinical manifestations of atopy. It is one of the most common chronic inflammatory skin diseases with increasing prevalence over the last century. The aetiology of this disease is multifactorial with a complex interaction of genetic, environmental and immunologic factors.
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5

Saramago, Eduardo Alves. "O hidrogênio molecular potencializa a hipotermia e previne a hipotensão e a febre durante a inflamação sistêmica induzida por LPS". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17134/tde-07022019-140036/.

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O hidrogênio molecular (H2) exerce efeito antioxidante, anti-apoptótico e antiinflamatório. Nesse estudo testamos a hipótese que o H2 modula as mudanças cardiovasculares, inflamatórias e termorregulatórias na inflamação sistêmica (IS) induzida por lipopolissacarídeo (LPS) em diferentes doses (0,1 ou 1,5 mg/kg, intravenoso, induzindo IS moderada ou severa) em ratos machos Wistar (250-300 g). LPS ou salina foi injetada imediatamente antes do início dos 360 minutos de inalação do H2 (2% H2, 21% O2, balanceado com nitrogênio) ou ar ambiente (21% O2, balanceado com nitrogênio). A temperatura corporal (Tc) foi mensurada por datalogger pré-implantados na cavidade peritoneal. O H2 não causou mudança nos parâmetros cardiovasculares, inflamatórios e na Tc dos ratos controle (tratados com salina). Durante a IS moderada o H2 reduziu o surgimento das citocinas pró-inflamatórias no plasma (TNF-? e IL-6) enquanto causou um aumento da IL-10 plasmática (citocina anti-inflamatória) e preveniu a febre. Durante a IS severa o H2 potencializou a hipotermia e preveniu a febre e a hipotensão. Além disso, o H2 causou uma redução no surgimento das citocinas pró-inflamatórias (TNF-? e IL-1? do plasma) e prostaglandina E2 [(PGE2), no plasma e no hipotálamo], e um aumento da IL-10 plasmática. Esses dados são consistentes com o entendimento que o H2 atenua a febre na IS moderada e durante a IS severa potencializa a hipotermia, previne a hipotensão e exerce um efeito antiinflamatório forte o suficiente para prevenir a febre alterando a sinalização febrigênica e alterando a produção hipotalâmica de PGE2
Molecular hydrogen (H2) exerts anti-oxidative, anti-apoptotic, and anti-inflammatory effects. Here we tested the hypothesis that H2 modulates cardiovascular, inflammatory, and thermoregulatory changes in systemic inflammation (SI) induced by lipopolysaccharide (LPS) at different doses (0.1 or 1.5 mg/kg, intravenously, to induce mild or severe SI) in male Wistar rats (250-300 g). LPS or saline was injected immediately before the beginning of 360- minute inhalation of H2 (2% H2, 21% O2, balanced with nitrogen) or room air (21% O2, balanced with nitrogen). Deep body temperature (Tb) was measured by dataloggers preimplanted in the peritoneal cavity. H2 caused no change in cardiovascular, inflammatory parameters, and Tb of control rats (treated with saline). During mild SI, H2 reduced plasma surges of proinflammatory cytokines (TNF-? and IL-6) while caused an increase in plasma IL-10 (anti-inflammatory cytokine) and prevented fever. During severe SI, H2 potentiated hypothermia, and prevented fever and hypotension. Moreover, H2 caused a reduction in surges of proinflammatory cytokines (plasma TNF-? and IL-1?) and prostaglandin E2 [(PGE2), in plasma and hypothalamus], and an increase in plasma IL-10. These data are consistent with the notion that H2 blunts fever in mild SI, and during severe SI potentiates hypothermia, prevents hypotension and exerts anti-inflammatory effects strong enough to prevent fever by altering febrigenic signaling and ultimately down-modulating hypothalamic PGE2 production
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Vale, Mariana Lima. "Atividade analgesica das interleucinas 4, 10 e 13 (IL-4, IL-10 e il-13) na dor inflamatoria experimental : papel de celulas residentes e citocinas". reponame:Repositório Institucional da UFC, 2000. http://www.repositorio.ufc.br/handle/riufc/2569.

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VALE, Mariana Lima. Atividade analgesica das interleucinas 4, 10 e 13 (IL-4, IL-10 e il-13) na dor inflamatoria experimental : papel de celulas residentes e citocinas. 2000. 140 f. Dissertação (Mestrado em Farmacologia) - Universidade Federal do Ceará. Faculdade de Medicina, 2000.
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The release of cyclo-oxigenase products and sympathomimetics amines, the final mediators of inflammatory pain, is preceded by the generation of cytokines by resident cells. In recent years a number of cytokines such as IL-4, IL-10, IL-13, IL-6, TGF-β e IFN-α have been described to inhibit the production of TNF-α, IL-1β, IL-6 and IL-8 (cytokines regarded as pró-inflammatory) and possibly to exert their modulatory effect on macrophages and mast cells. Since it is known the capacity of those cytokines to inhibit the production of pro-inflammatory cytokines and the pivotal role of resident cells in the development of inflammatory pain we have decided to test the possibility of IL-4, IL-13 and IL-10 to modulate inflammatory pain. In short, IL-4 (1 – 5ng/animal), IL-13 (0.4 - 2.5ng/animal) or IL-10 (0.4 - 10ng/animal) was given 30 min before acetic acid (AAc) or zymosan (Zym) administration in the writhing model. IL-4 (2.5 e 5 ng/animal), IL-13 (1 e 2.5 ng/animal) or IL-10 (2 e 10 ng/animal) were injected, ip, 30 min before Zym (1 mg/animal; intra-articular) in the rat knee joint incapacitation test up to the 4th hour (the number of leukocytes was determined in the articular exsudate 6 hours later). Doses of those cytokines that exerted maximum effect in the writhing test were also injected 30 min before the hot plate test. These same doses were injected ip before naloxone administration in the AAc-induced writhing model in mice. TNF-α and IL-1β were determined in the supernatant of a macrophage culture which were collected from peritoneal fluid of mice treated with Zym and pre-treated with the cytokines under test. Our results show that interleukins 4, 13 and 10 inhibit writhing response in mice induced by AAc or Zym up to 58.7, 89.2 and 52%, and up to 62.6, 61.7 and 74.4%, respectively (p<0.05). Similar results were observed in the rat knee joint incapacitation test induced by Zym: 49.2, 56.6, 69,9% of inhibition (p<0.05). The same interleukins were able to inhibit Zym-induced leukocyte influx into articular cavity (53.8, 92.1 e 62% of inhibition, respectively - p<0,05). The analgesic activity of IL-4, IL-13 and IL-10 seems to be peripheral, since these cytokines presented no effect in the reaction time of the animals on hot plate test. This antinociceptive effect seems to have no relation with endogen opioid release since naloxone (opioid receptor antagonist) had no effect in reverting the antinociceptive effect of cytokines in the AAc-induced writhing in mice. However, IL-4 and IL-10 inhibit the release of TNF-α (42 e 41.2%, respectively - p<0.05) and of IL-1β (61.9 e 80.9%, respectively - p<0,05) by macrophages stimulated in vivo by Zym, indicating that their antinociceptive activities may be due to the inhibition of those cytokines release by resident cells.
Já está estabelecido que a liberação de produtos da cicloxigenase e aminas simpatomiméticas, mediadores finais da dor inflamatória é precedido pela geração, por células residentes, de uma cascata de citocinas. Recentemente dados do nosso laboratório demonstraram que no modelo de contorções abdominais (CA) a ativação dessa cascata é dependente também da presença de células residentes como macrófagos e mastócitos. Dados da literatura apontam algumas citocinas capazes de modular negativamente a função dessas células: IL-4,. IL-10, IL-13, IL-6, TGF-β e IFN-α . Com base nesses dados, o objetivo do presente trabalho foi estudar uma possível atividade analgésica de três citocinas: IL-4, IL-13 e IL-10. Para tanto injetou-se, via ip, IL-4 (1–5ng/animal), IL-13 (0.4-2.5ng/animal) ou IL-10 (0.4-10ng/animal) 30 min antes da administração de zymosan (Zym) ou ácido acético (AAc) para o teste de CA. IL-4 (2.5 e 5ng/animal), IL-13 (1 e 2.5ng/animal) ou IL-10 (2 e 10ng/animal) foi injetada, ip, 30 min antes do Zym (1 mg/animal; intra-articular) e logo após foi medida a incapacitação articular (IA) até a 4ª hora e na 6ª hora foi feita a contagem de leucócitos no fluido articular. As interleucinas estudadas também foram administradas (30 min antes) na dose que melhor inibiu as CA no teste da placa quente (PQ) e em camundongos que haviam recebido ou não a naloxona previamente ao estímulo (AAc) no teste de CA. IL-4 (5 ng/animal) ou IL-10 (10 ng/animal) foi injetada ip 30 min antes do Zym (ip) e após 15 min os animais foram sacrificados e o exsudato peritoneal foi colhido e posto em cultura para a dosagem de IL-1β e TNF-α no sobrenadante. No presente trabalho ficou demonstrado que as interleucinas-4, 13 e 10 são analgésicas tanto no modelo de CA induzidas por AAc (58.7, 89.2, 52% de inibição, efeito máximo, respectivamente, p<0.05) ou Zym (62.6, 61.7, 74.4% de inibição, efeito máximo, respectivamente, p<0.05) como também no modelo de IA induzido por Zym (49.2, 56.6, 69,9% de inibição, efeito máximo, respectivamente, p<0.05). As citocinas estudadas foram capazes de inibir o influxo de leucócitos para a cavidade articular (53.8, 92.1 e 62%, respectivamente - p<0,05). Foi demonstrado que o efeito analgésico parece ser de domínio periférico visto que nenhuma das citocinas modificou o tempo de reação na PQ, teste algesimétrico sensível apenas para drogas que exercem efeito central. Também foi demonstrado que a atividade analgésica das interleucinas testadas não depende da liberação de opióides endógenos, visto que o pré-tratamento com naloxona não foi capaz de reverter a atividade analgésica de nenhuma das interleucinas no modelo de CA. Contudo essa atividade analgésica parece depender da inibição da liberação de citocinas por células residentes visto que IL-4 e IL-10 foram capazes de diminuir a liberação de TNF-α (42 e 41.2% de inibição respectivamente - p<0.05) e IL-1β (61.9 e 80.9% de inibição respectivamente - p<0,05) por macrófagos peritoneais residentes.
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Costa, Tânia Alves da. "A função da IL-10 na paracoccidioidomise pulmonar murina". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-16122010-113911/.

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O principal mecanismo de defesa de hospedeiros infectados pelo Paracoccidioides brasiliensis (Pb), fungo dimórfico que causa a mais importante micose sistêmica da América Latina, é a imunidade celular. Neste processo participam macrófagos ativados por IFN-g e a IL-10 parece ser a citocina que se contrapõe a esta ativação. Tanto na patologia humana como em modelos experimentais há fortes indicações de que a IL-10 age como supressora da imunidade celular causando efeitos deletérios aos hospedeiros; entretanto, estudos diretos sobre a função da IL-10 na paracoccidiodomicose (PCM) não tinham sido ainda realizados. Então o objetivo fundamental deste trabalho foi estudar a função da IL-10 nos mecanismos da imunidade inata e adaptativa contra o Pb utilizando como modelo experimental camundongos geneticamente deficientes de IL-10 (IL-10 nocaute, IL-10 KO) em comparação com seus controles normais (WT). Demonstramos in vitro que macrófagos peritoneais normais de camundongos IL-10 KO apresentam uma maior atividade fagocítica e fungicida que os macrófagos de camundongos WT e isto esteve associado à maior produção de IFN-g, TNF-α, óxido nítrico (NO) e da quimiocina MCP-1. Verificamos, entretanto, que a produção de IFN-g era realizada por células NKT contaminantes de macrófagos aderentes nos camundongos IL-10 KO, sugerindo uma possível participação destas células na ativação de macrófagos e de células T de camundongos IL-10 KO. Estudos in vivo revelaram que a partir da 2ª semana de infecção os camundongos IL-10 KO apresentaram uma resposta imune precoce em relação aos WT, pois os pulmões dos primeiros apresentavam carga fúngica significativamente menor, associada com aumento da maioria dos isótipos de anticorpos (IgM, IgG1, IgG2a, IgG2b) específicos contra o fungo. Observamos também a inibição total da produção das citocinas IL-4 e IL-5, mostrando a ação reguladora da IL-10 na síntese de citocinas Th2. Na 4ª semana pós-infecção a carga fúngica continuou menor nos animais IL-10 KO, mas não foram observadas as diferenças quanto à síntese de anticorpos entre as duas linhagens. A análise dos leucócitos infiltrantes nos pulmões revelou um aumento na frequência de linfócitos T CD4+ ativados nos camundongos IL-10 KO em relação aos WT. A partir da 8ª semana, a carga fúngica pulmonar dos camundongos IL-10 KO reduziu consideravelmente e não ocorreu disseminação para outros órgãos. Observou-se também, nesta linhagem, um aumento na resposta de hipersensibilidade do tipo tardio (HTT), confirmando o padrão de resposta desviado para um perfil Th1. A análise histológica dos órgãos dos camundongos IL-10 KO revelou ausência de granulomas e fungos no pulmão em contraste aos seus controles WT que apresentavam elevado número de granulomas e fungos neste órgão. A análise dos linfócitos infiltrantes nos pulmões dos camundongos IL-10 KO mostrou redução na frequência de células B, o que é coerente com a baixa síntese de anticorpos observada. Houve aumento marcante na freqüência de células T CD4+ e T CD8+ memória/efetora, caracterizando mais uma vez a eficiente resposta imune celular nesses animais associada à ausência do papel regulador negativo da IL-10. Em fase mais tardia (16 semanas pós-infecção) a regressão da infecção nos camundongos IL-10 KO continuou evidente pelo pequeno número de fungos recuperados do pulmão, acompanhada de baixa síntese de citocinas (IL-5 e IL-2) e de anticorpos anti- P. brasiliensis. Na 23ª semana de infecção além da baixa carga fúngica nos camundongos IL-10 KO, associada à baixa frequência de células responsáveis pela imunidade celular ocorreu também redução na freqüência de células Treg, indicando o papel regulador da IL-10 nesta subpopulação celular. A elevada sobrevida (90%) dos animais IL-10 KO foi coerente com a baixa carga fúngica e eficiente resposta imune no curso da infecção. Em conjunto, nosso trabalho demonstra o importante papel regulador da IL-10 na imunidade da PCM.
Cellular immunity is the main defense mechanism of hosts infected by the Paracoccidioide brasiliensis (Pb), a dimorphic fungus that causes the most important systemic mycosis in Latin America. IFN-g activated macrophages participate in this activity that is antagonized by IL-10 an anti-inflammatory cytokine. Both, in the human pathology and in experimental models, there are a number of evidences indicating that IL-10 acts as a suppressor of cellular immunity leading to deleterious effects to the hosts. However, direct studies aimed at investigating the function of IL-10 in the immunity to paracoccidioidomycosis (PCM) have not been performed. Thus, the fundamental objective of this work was to study the function of IL-10 in the mechanisms of innate and adaptive immunity against Pb using as experimental model IL-10 deficient mice (IL-10 Knockout, IL-10 KO) compared to their respective wild type (WT) controls. We demonstrated in vitro that normal peritoneal macrophages of IL-10 KO mice presented increased phagocytic and microbicidal activities than macrophages of WT mice and this was associated witch an elevated production of IFN-g, TNF-α, nitric oxide (NO) and the chemokine MCP-1. However, the production of IFN-g seen to be performed by NTK cells contaminating adherent macrophages, suggesting a possible participation of these cells in the activation of macrophages and T cells of IL-10 KO mice. In vivo studies revealed that at the second week of infection IL-10 KO mice presented an earlier immune response when compared to wild-type mice, since their lungs exhibited a significantly reduced fungal burden and an increased production of almost all antibodies isotypes (IgM, IgG1, IgGM, IgG2b). This effect was accompanied by a total absence of IL-4 and IL-5, showing a regulatory action of IL-10 in the synthesis of Th2 cytokines. Four weeks post-infection, the fungal load was still lower in the IL-10 KO mice but no differences in antibody synthesis was observed. However, the analysis of lung infiltrating leukocytes revealed an increased frequency of TCD4+ and TCD4+CD44 high lymphocytes in IL-10 KO mice, again demonstrating an early activation of cellular immunity in IL-10 KO mice. When compared with WT mice, the pulmonary fungal loads of IL-10 KO mice at week 8 of infection were drastically reduced and no dissemination to other organs were observed. The histopathological analysis revealed an absence of granulomas and fungi in the lungs of IL-10 KO in comparison with WT mice. The analysis of lung infiltrating leukocytes showed that IL-10 KO mice had a reduction in the frequency of B cells, in agreement with the reduced synthesis of immunoglobulins. An increased frequency of activated T CD4+ and a drastic increase of TCD4+ and T CD8+ effector/memory cells charactering once again an efficient immune response associated with IL-10 deficiency. In later stages, sixteen weeks after infection, a regressive infection of IL-10 KO mice was further characterized by low numbers of fungi in the lung, reduced synthesis of cytokines (IL-4 and IL-5) and anti- P. brasiliensis antibodies. By week 23 after infection, in addition to the characteristic reduction of fungal loads and reduced frequency of immune cells, we observed a decrease in the frequency of Treg cells, demonstrating the implication of IL-10 in the control of this T cell population. The elevated survival (90%) of IL-10 KO mice was in total agreement with the low fungal burdens and efficient immune response observed during infection. In conclusion, our work demonstrates for the first time that IL-10 plays a major role in the control of innate and adaptive immunity to Pb infection.
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Cirocco, Robert E. "Cytokine analisys in atlantic bottlenose dolphins: molecular characterization of IL-4, IL-6, and IL-10". FIU Digital Commons, 2001. http://digitalcommons.fiu.edu/etd/2370.

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The health status of wild and captive Atlantic Bottlenose dolphins (Tersiops truncatis) is difficult to ascertain. Mass strandings of these animals have been attributed to pollutants, as well as bacterial infections. Using human Enzyme Linked Immuno-Assays (ELISA) for immunological cytokines, I measured soluble cytokine levels with respect to their health status. In a retrospective analysis of dolphin sera, there was a trend of higher cytokine levels in “sick” animals. I cultured dolphin lymphocytes in the presence of a mitogen (PHA), a super antigen (Staph-A), Lipopolysaccharide (LPS), and a calcium flux inducer (PMA). Levels of messenger RNA, from these cultured cells, were assayed with Polymerase Chain Reaction (PCR) using primers for the human cytokines IL-2, EL-4, IL- 6, IL-10, Tumor Necrosis Factor, and Interferon gamma. Only IL-4, IL-6, and IL-10 messages were obtained, inferring similar nucleotide homology to the human primer sequences. The PCR products were sequenced. Sixteen IL-4 sequences, twelve IL-6 sequences and seven IL-10 sequences were obtained and analyzed. Each cytokine exhibited the same nucleotide sequence in all dolphins examined. There was no difference in the cytokine profile in response to the various stimuli. The derived amino acid composition for each of the dolphin cytokines was used for molecular modeling, which showed that dolphin IL-4, IL-6, and IL-10 were structurally similar to the corresponding proteins of Perissodactyla.
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9

Mitchell, Ruth Elizabeth. "Regulation of IL-10 in CD4+ T cells". Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.691167.

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OLIVEIRA, Gabriela Almeida de. "Polimorfismos de citocinas (TNF-A, IL-10 e IL-17) no câncer gástrico". Universidade Federal do Pará, 2016. http://repositorio.ufpa.br/jspui/handle/2011/7251.

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FADESP - Fundação de Amparo e Desenvolvimento da Pesquisa
No Norte do Brasil, o câncer gástrico (GC) é a segunda neoplasia mais frequente entre os homens e o terceiro nas mulheres, portanto, um importante problema de saúde pública. A investigação de fatores genéticos relacionados com características imunológicas pode auxiliar o entendimento da carcinogênese no CG. O objetivo do presente trabalho foi polimorfismos presentes nos genes das interleucinas IL17G-197A, IL 17FA7488G, TNFαG-308A, IL10G- 1082A, IL10C-819T e IL10C-592A, em amostras de pacientes com câncer gástrico e sem câncer. O grupo caso foi composto por 100 pacientes diagnosticados com CG, atendidos no Hospital HUJBB (Pará, Brasil). O grupo controle foi constituído de 100 indivíduos, não aparentados, sem câncer da mesma população. O material genético foi extraído a partir de 5 mL de sangue periférico pelo kit comercial de DNA da Roche, seguido de quantificação com o NanoDrop 1000 spectrophotometer. Molecular analysis of the polymorphisms was performed by real-time PCR with TaqMan® probes. E as medidas de ancestralidade foram investigadas utilizando um painel de 48 marcadores autossômicos informativos de ancestralidade (AIMs). As proporções de ancestralidade de Europeu, Africano e Ameríndio foram estimadas usando o software STRUCTURE v.2.3.3. Como resultado, observou-se que a composição étnica do grupo com câncer foi de 27% africano, 42% europeu, e 31% de ameríndia. No grupo sem câncer, a composição foi de 21 % africano, 52% europeia, e 27% de ameríndia. Em relação ao conjunto de marcadores da interleucina IL-10 (IL10G-1082A, IL10C-819T, IL10C-592A), quando comparados os padrões genotípicos e haplotípicos observou-se que a distribuição haplotípica, quando relacionada a elevada expressão (GCC/GCC, GCC/GCA, GCC/GTC, GCA/GCA, GCA/GTA) foi mais frequente no grupo de pacientes com câncer gástrico (p=1,15E-11; OR=2,630; IC 95%=2,116-3,271). Em indivíduos que possuíam o genótipo relacionado com a elevada produção de IL-10, detectou-se maior frequência da ancestralidade europeia no grupo de indivíduos controle (p=1E-06), enquanto no grupo de pacientes com CG observou significante frequência da ancestralidade africana (p=1.4 e-5), pacientes que apresentaram genótipos TNF-α AA e TNF-α AG para mutação no gene TNF-α, apresentam risco elevado para desenvolvimento do câncer (P <000.1; OR 10.375; IC 95% 3.149- 34.061). Concluimos que a distribuição haplotípica dos marcadores da interleucina IL-10 (IL10G-1082A, IL10C-819T, IL10C-592A) quando relacionados a elevada expressão e predominância de ancestralidade africana, possuem maior risco de desenvolvimento do CG.
Gastric cancer (GC) is the second most common malignancy among men and the third in women, and therefore, an important public health problem in northern Brazil. The investigation of genetic factors related to immunological characteristics can aid the understanding of carcinogenesis in CG. The objective of the present work was investigate polymorphisms present in interleukin genes IL17G-197A, IL 17FA7488G, TNFαG-308A, IL10G-1082A, IL10C-819T e IL10C-592A, on samples of patients with gastric cancer and healthy patients without cancer. Case group was composed of 100 patients diagnosed with CG, met in the Hospital HUJBB (Pará, Brazil). Control group was composed of 100 individuals without cancer, unrelated, of the same population. The genetic material was extracted from 5 mL of peripheral blood with the DNA commercial kit from Roche, followed by quantification with the NanoDrop 1000 spectrophotometer. Analysis of the molecular polymorphisms was performed by real-time PCR with Taqman® probes. Measures of ancestry were investigated using a panel of 48 autosomal ancestry informative markers (AIMs). The proportions of ancestry of European, African and Amerindian were estimated using the software STRUCTURE v. 2.3.3. It was observed that the ethnic composition of the case group was 27% African, 42% European and 31% of Amerindian, while in the control group 21% African, 52% of European and 27% of Amerindian. In relation to the set of markers of interleukin IL-10 (IL10G-1082A, IL10C-819T, IL10C-592A), when the genotypic and haplotypic patterns were compared, it was noted that the haplotype distribution related to high expression (GCC/GCC, GCA, GCC/GCC/GTC, GCA/GCA, GCA/GTA) was more frequent in the patients with gastric cancer (P = 1,15e-11; OR = 2.630; IC 95% = 2.116-3.271). Among the individuals with the genotype related to the high production of IL-10, it was observed that the control group had more European contribution in their ancestry (P = 1e-06) while the group of patients with CG had more African contribution in their ancestry (P = 1.4e-5). Patients who presented TNF-α AA and TNF-α AG genotypes for TNF-α gene mutation presented a higher risk for development of cancer (P<0.001; OR 10.375; IC 95% 3.149-34.061). It is concluded that patients with a distribution of haplotypic markers of interleukin IL-10 (IL10G-1082A, IL10C-819T, IL10C-592A) related to a higher expression and higher contribution of African ancestry have a high risk of developing gastric cancer.
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Libri sul tema "IL-10"

1

Grossi, Plinio. Il Ticino dei '10. Pregassona: Fontana, 1997.

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Gordon, Yefim. Ilyushin IL-2 and IL-10 Shturmovik. Ramsbury: Crowood, 2004.

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Costa, Manuel Rui. Il mio 10 per Firenze. [Italy]: AN.MA & San Marco Sport Events, 1998.

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Mübariz, Qurbanlı, e Ălii̐ev Ilgar, a cura di. Yeni Azärbaycan Partiyası 10 il. Bakı: Azarbaycan, 2002.

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5

Castel nuovo (Museum : Naples, Italy), a cura di. Il Futurismo: Anni '10 - anni '20. Milano: Skira, 2018.

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Chiara, Piero. Il Decameron raccontato in 10 novelle. Milano: A. Mondadori, 1992.

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7

Paek, Tʻae-wŏn. Paek Tʻae-wŏn kongye chakpʻumjŏn: 1985-yŏn 10-wŏl 10-il--16-il Tongbang Pʻŭllaja Misulgwan. [Seoul]: Kabŭl, 1985.

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Kim, Chŏng-il. Misullon: 1991-yŏn 10-wŏl 16-il. [Pʻyŏngyang]: Chosŏn Nodongdang Chʻulpʻansa, 1992.

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Kim, Chŏng-il. Misullon: 1991-yŏn 10-wŏl 16-il. [Pʻyŏngyang]: Chosŏn Nodongdang Chʻulpʻansa, 1992.

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10

Hanʼgŭl mit Hanʼgugŏ Chŏngbo Chʻŏri Haksul Taehoe (4th 1992 Hanʼguk Tʻongsin Yŏnʼgu Sentʻŏ). Inʼgan kwa kigye wa ŏnŏ: Ilsi 1992-yŏn 10-wŏl 9-il - 10-il, changso Hanʼguk Tʻongsin Yŏnʼgu Sentʻŏ. Sŏul-si: Hanʼguk Chŏngbo Kwahakhoe, 1992.

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Capitoli di libri sul tema "IL-10"

1

Benjamin, David. "Interleukin-10 (IL-10)". In Cytokines: Interleukins and Their Receptors, 305–19. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-1241-3_12.

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Engelhardt, Karin R., e Bodo Grimbacher. "IL-10 in Humans: Lessons from the Gut, IL-10/IL-10 Receptor Deficiencies, and IL-10 Polymorphisms". In Current Topics in Microbiology and Immunology, 1–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-43492-5_1.

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Lee, Myung-Shik, e Nora Sarvetnick. "IL-10 Transgenic Mice". In Interleukin-10, 135–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_15.

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Shanmugam, Saravanan, Jullyana S. S. Quintans, Parimelazhagan Thangaraj, Luciana Scotti, Marcus T. Scotti, Adriano A. S. Araújo e Lucindo J. Quintans-Júnior. "Monoterpenes Modulating IL-10". In Phytomedicine, 157–68. First edition. | Boca Raton, FL : CRC Press, 2020.: CRC Press, 2020. http://dx.doi.org/10.1201/9781003014898-16.

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Carvalho, Edgar M. "IL-10 In Human Leishmaniasis". In Interleukin-10, 91–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_10.

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Sieling, Peter A., e Robert L. Modlin. "IL-10 in Mycobacterial Infection". In Interleukin-10, 79–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_9.

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Schroeder, John T. "Diagnostic Components: T Helper Cell Cytokines (IL-4, IL-5, IL-9, IL-10, IL-13, IL-17)". In Encyclopedia of Medical Immunology, 221–26. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9194-1_298.

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Schuitemaker, Hanneke, Neeltje A. Kootstra e Frank Miedema. "IL-10 and HIV-1 Replication". In Interleukin-10, 101–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_11.

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Yssel, Hans, e René de Waal Malefyt. "IL-10 and Human T Cells". In Interleukin-10, 19–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_3.

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10

Van Vlasselaer, Peter. "IL-10 and Bone Formation/Hematopoiesis". In Interleukin-10, 59–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22038-2_7.

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Atti di convegni sul tema "IL-10"

1

Darmaputra, I. Gusti Nyoman, Luh Mas Rusyati, Wibi Riawan, Anang Endaryanto e Cita Rosita Sigit Prakoeswa. "The Correlation between Neutrophil CD64, Interleukin-17 (Il-17), Interleukin-10 (Il-10) in Skin Tissue and Neutrophil CD64, Il-17 and Il-10 in Blood Circulation in Erythema Nodosum Leprosum (ENL) Patients". In The 23rd Regional Conference of Dermatology 2018. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0008155802860290.

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Khan, Aslam A. "Abstract 387: PEDF binds to IL- 10 receptor in the absence of IL-10 and inhibits melanoma tumor growth". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-387.

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Gollnick, Sandra O., David A. Musser e Barbara W. Henderson. "Photodynamic therapy affects the expression of IL-6 and IL-10 in vivo". In BiOS '98 International Biomedical Optics Symposium, a cura di Steven L. Jacques. SPIE, 1998. http://dx.doi.org/10.1117/12.308168.

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Cerri, S., M. Gold, J. Jin, T. Robinson, S. Thompson, S. Smyk-Pearson, DA Lewinsohn e DM Lewinsohn. "Human IL-10 Producing T Cells Specific forMycobacterium tuberculosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5907.

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Senturk, T., BG Cetin e N. Aydin. "315 The relationship between il-10, il-17, il-23 and vitamin d levels, and disease activity of systemic lupus erythematosus". In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.315.

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Sato, K., Y. Aizaki, H. Yazawa e T. Mimura. "AB0066 Combination of il-10 and il-18 but not il-6 and il-18 induces ifn-gamma production and surface expression of trail on nk cells". In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3407.

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Cai, J., G. Su, X. Qi, A. Emtiazjoo, P. A. Efron, M. Brantly, B. Mehrad et al. "Myeloid-Derived Suppressor Cells Ameliorate Lung Ischemia-Reperfusion Injury Via Regulation of IL-17 and IL-10". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1002.

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Orellana, C., R. Sanmartí, JD Cañete, J. Yagüe, G. Ercilla, A. Gómez, G. Salvador e J. Muñoz-Gómez. "THU0002 Il-10 and il-6 polymorphisms are not related to erosive disease in early rheumatoid arthritis". In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.105.

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Radbruch, AH, M. Loehning, A. Richter, T. Stamm, O. Soezeri, HD Chang, L. Tykocinski e M. Assenmacher. "THU0051 Proliferation and stability of cytokine expression of il-4 or il-10 secreting t helper cells". In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.848.

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Terai, Mizue, Masumi Eto, Garbo D. Young, Michael J. Mastrangelo, Yutaka Tamura, Kenichi Harigaya e Takami Sato. "Abstract 1913: Proinflammatory cytokine, Interleukin-6 (IL-6), promotes Interleukin-10 (IL-10) production from melanoma cell via JAK/STAT3 and Raf/ERK signal pathways". In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1913.

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Rapporti di organizzazioni sul tema "IL-10"

1

Petkova, Boryana, Emilia Alova, Iliya Karagyozov, Polya Stoyanova, Vladimir Jekov, Milena Mourdjeva e Tsvetelina Oreshkova. IL-10: a Potential Prognostic Biomarker for Missed Abortion. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, luglio 2019. http://dx.doi.org/10.7546/crabs.2019.07.16.

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2

Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang e Chenming Xu. Association of IL-4 and IL-10 Polymorphisms with Preterm Birth Susceptibility: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.

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Review question / Objective: The aim of our systematic review and meta-analysis was to summarize the effects of IL-4 and IL-10 gene polymorphism and clarify their possible association with PTB. Condition being studied: World Health Organization (WHO) defines preterm birth (PTB) as babies born alive before 37 weeks of pregnancy are completed. The new estimates show that the prevalence of PTB during 2014 ranged from 8.7% to13.4% of all live births, about 15 million preterm babies born each year. Besides, PTB is the leading cause of death worldwide for children below 5 years of age. Babies born preterm are at an increased risk of short-term and long-term complications attributed to immaturity of multiple organ systems, such as cerebral palsy, intellectual disabilities, vision and hearing impairments, and impaired cognitive development. PTB has become a worldwide public health problem, but its etiology remains unclear. Accumulating evidence shows that PTB is a syndrome that can be attributed to a variety of pathological processes(5). Inflammatory diseases and genetic background are known risk factors for PTB, many studies had shown that genetic variations in proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 α (IL-1 α) are associated with increased risk of PTB, but the relationship between genetic polymorphism in anti-inflammatory cytokines and risk of PTB remains controversial.
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3

Grigorov, Boncho G., Anastasiya G. Trenova, Georgi S. Slavov, Lyuba D. Miteva e Spaska A. Stanilova. Interleukin‑10 (IL‑10) Promoter Polymorphism at Position –1082 in Bulgarian Patients with Multiple Sclerosis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, febbraio 2019. http://dx.doi.org/10.7546/crabs.2019.01.11.

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4

Jafrin, Sarah, Md Abdul Aziz e Mohammad Safiqul Islam. Elevated levels of pleiotropic interleukin-6 (IL-6) and interleukin-10 (IL-10) are critically involved with the severity and mortality of COVID-19: An updated longitudinal meta-analysis and systematic review on 147 studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, aprile 2022. http://dx.doi.org/10.37766/inplasy2022.4.0046.

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Review question / Objective: How were serum IL-6 and IL-10 linked with the severity and mortality of COVID-19 patients? To evaluate the role of IL-6 and IL-10 in the development of the severity or morality of COVID-19 patients. The outcomes (mean difference) were calculated between the severe vs. non-severe COVID-19 patients and non-survival vs. survival patients to evaluate the risk of severity or mortality. Condition being studied: Severity and mortality among the COVID-19 patients. Information sources: The international scientific authorized databases such as Google Scholar, PubMed, Embase, CNKI, Cochrane Library, and Web of science were used as primary sources to identify and collect the eligible literature. Additional secondary databases were also comprehensively searched to extract more related studies.
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5

Splitter, Gary, Zeev Trainin e Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, luglio 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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6

Tillett, Will, e Oliver Jones. Améliorer l’assainissement rural dans les contextes difficiles. The Sanitation Learning Hub, Institute of Development Studies, marzo 2021. http://dx.doi.org/10.19088/slh.2021.021.

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Sur les deux milliards de personnes au monde qui vivent sans accès à, au moins, un assainissement de base, sept sur dix vivent en milieu rural. Des progrès ont été faits pour accroître l’assainissement rural et les niveaux d’accès augmentent, toutefois, il reste difficile d’atteindre le « dernier kilomètre » soit les 10 à 20 pour cent de la population qui vivent dans les contextes les plus rudes. Les facteurs qui affectent la capacité des ménages à construire et utiliser des toilettes, ainsi que les difficultés auxquelles sont confrontés les programmes d’assainissement pour atteindre des groupes spécifiques sont extrêmement variés. Il est prouvé que l’adoption d’approches universelles ne donne pas de bons résultats ; par conséquent, il nous faut des approches plus nuancées, adaptées et ciblées pour refléter l’universalité des Objectifs de développement durable (ODD) et faire en sorte que personne ne soit laissé de côté. Toutefois, nous reconnaissons que les difficultés peuvent être persistantes et qu’il n’existe que peu d’exemples documentés sur la manière de les surmonter de manière systématique. La Sanitation Learning Hub, l’UNICEF et WaterAid ont commandité cette étude pour cartographier les approches d’assainissement rural dans des contextes difficiles et les conseils actuellement prodigués, et pour recenser les expériences et enseignements qui s’en dégagent. Elle a englobé des entretiens avec 44 informateurs clés (EIC) et la consultation de plus de 180 ressources documentaires. Cette Note d’apprentissage donne une vue d’ensemble des conclusions de l’étude.
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7

Li, Zifeng, Yuling Fan, Yunhong Lei, Xiaoqiang Hou e Caiyun Chang. A protocol for systematic review and network meta-analysis Efficacy and Safety of Kunxian Capsule in Treating Patients with Lupus Nephritis：A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, dicembre 2021. http://dx.doi.org/10.37766/inplasy2021.12.0005.

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Review question / Objective: To study on the efficacy and safety of Kunxian Capsule in treating patients with lupus nephritis( LN). Condition being studied: The study showed that Kunxian capsule significantly improved immune status and renal function and suppressed IL-10 and TNF in serum of lupus mice- α Of secretion, works better in combination with and reduces hormone dosage. At present, there are few studies in which Kunxian capsules are used in the clinic, and the conclusions of the studies are inconsistent, so this study was conducted in order to comprehensively evaluate the efficacy and safety of Kunxian capsules for the treatment of lupus nephritis.
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8

Liu, Miao, Hongan Wang, Jing Lu, Zhiyue Zhu, Chaoqun Song, Ye Tian, Xinzhi Chen et al. Vitamin D supplementation in the treatment of Myasthenia Gravis A protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, settembre 2022. http://dx.doi.org/10.37766/inplasy2022.9.0129.

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Review question / Objective: The patients should meet the internationally recognized diagnostic criteria for myasthenia gravis and be definitely diagnosed as myasthenia gravis, excluding MG patients caused by congenital, drug and other factors, as well as patients with serious primary diseases, autoimmune diseases or mental diseases. Patients are not restricted by race, region, gender, age, background, course of disease and other factors. We will focus on trials using vitamin D as an intervention at any dose and in any regimen (eg daily/weekly/monthly intake). The control group was routinely given western medicine, including cholinesterase inhibitors, glucocorticoids, immunosuppressants, alone or in combination, or placebo. The intervention group was treated with vitamin D on the basis of western medicine treatment in the control group. The specific dosage form and dose were not limited, and the shortest course of treatment should be 4 weeks. Main outcome measures: (1) Quantitative score of myasthenia gravis (QMG); (2) Recurrence rate; (3) Effective. Secondary outcome measures: (1) The level of serum acetylcholine receptor antibody (AchRab); (2) The levels of inflammatory factors such as IL-6 and IL-10; (3) Clinical absolute score; (4) TCM syndrome score scale; (5) Quality of life score (QOL); (6) Incidence rate of adverse events. All randomized controlled trials (RCT) literatures from the establishment to September 2022 were retrieved and classified.
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9

Ripoll, Santiago, Tabitha Hrynick, Ashley Ouvrier, Megan Schmidt-Sane, Federico Marco Federici e Elizabeth Storer. 10 façons dont les gouvernements locaux en milieu urbain multiculturel peuvent appuyer l’égalité vaccinale en cas de pandémie. SSHAP, gennaio 2023. http://dx.doi.org/10.19088/sshap.2023.001.

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Si l’on s’en tient aux chiffres de la vaccination contre la COVID-19 dans les pays du G7, la campagne apparaît comme un véritable succès tant au niveau global qu’au niveau national. En effet, à ce jour, 79,4 % de la population totale des pays du G7 a reçu une première dose, 72,9 % une seconde, et 45,4 % une dose de rappel (données du 28 avril 2022) 1 En France, c’est 80,6 % de la population totale qui a reçu une première dose, 78,2 % qui a reçu deux doses, et 55,4 % qui a reçu un rappel (données du 28 avril 2022).2 Au Royaume-Uni, 79,3 % de la population totale a reçu une première dose, 74,1 % une seconde, et 58,5 % un rappel.1 Enfin, en Italie, 85,2 % de la population totale a reçu une première dose, 80,4 % a reçu deux doses et 66,5 % a reçu leurs rappels (données du 28 avril 2022). Ces taux de vaccination élevés masquent pourtant des disparités importantes à l’intérieur de chaque pays. Ainsi, à Marseille, deuxième ville de France, moins de 50 % des habitants des quartiers nord de la ville étaient vaccinés à la fin de l’année 2021, alors que plus de 70 % des habitants des quartiers sud l’étaient au même moment.3 Dans le quartier populaire de Ealing, situé au nord-ouest de Londres, 70 % de la population admissible avait reçu une première dose, soit près de 10 % de moins que la moyenne nationale. 4 (Données du 4 avril 2022). Des disparités similaires ont été observées dans d’autres métropoles urbaines des pays du G7. Ce document examine ces disparités au prisme de la notion d’« (in)égalité vaccinale ». En s’appuyant sur des recherches qualitatives menées pendant la campagne de vaccination de la COVID-19 dans les quartiers nord de Marseille, le quartier de Ealing à Londres (Nord-ouest) et dans la région de l'Émilie-Romagne et à Rome, en Italie, il montre comment les autorités locales peuvent agir pour atténuer ces inégalités. Mieux comprendre les inégalités en matière de vaccins fut primordial lors de la pandémie de la COVID-19 en ce sens que les populations sous-vaccinées étaient la plupart du temps des minorités ethniques ou culturelles, vivant dans des zones défavorisées, ou sans-papiers, donc plus susceptibles de contracter la COVID-19, et d’en subir les conséquences les plus dramatiques. 5 6 7 8 Ainsi, à Ealing, quatre mois après la campagne de vaccination, seulement 57,6% des personnes dans le décile de pauvreté le plus bas avaient reçu une dose, contre 81% des personnes dans le décile le plus aisé. 9 En outre, 89,2 % des résidents britanniques blancs de Ealing étaient vaccinés, contre 64 % des Pakistanais et 49,3 % des habitants issus des Caraïbes.9 À Rome, comme c’est le cas dans d’autres métropoles urbaines des pays du G7, nos données révèlent des disparités particulières importantes entre le recours aux vaccins des populations sans papiers et celui des citoyens établis. Les facteurs d’inégalité vaccinale dans ces environnements urbains sont complexes et liés à l’interaction de nombreux phénomènes tels que les inégalités économiques, le racisme structurel, l'inégalité d'accès aux soins de santé, la méfiance envers les professionnels de santé, les représentants de l'État, et plus encore. Les collectivités locales tout comme les professionnels de la santé, les groupes communautaires et les résidents jouent un rôle clé dans la manière dont s’exprime l’(in)égalité vaccinale. Pour autant, peu de leçons ont été systématiquement tirées des efforts menés en matière d’ «engagement vaccinal » au niveau local. Dans ce document, nous proposons d’expliquer comment l’expérience des inégalités structurelles se recoupe avec celle des habitants, et comment ces expériences ont été prises en compte ou au contraire ignorées dans la promotion et l’administration des vaccins contre la COVID-19 par les collectivités locales. Nous adressons également un ensemble de recommandations qui s’appliquent aux programmes de « vaccination de rattrapage » contre la COVID-19 (visant à atteindre les personnes qui n’ont pas encore reçu leur schéma vaccinal complet), mais elles concernent également les programmes de vaccination d'urgence à venir. Ce document repose sur des recherches menées entre octobre et décembre 2021 à Marseille et sur des échanges réguliers avec les autorités du Borough de Ealing initiés dès mai 2021. Il identifie comment les gouvernements locaux, les acteurs de la santé, les groupes communautaires et les résidents jouent un rôle clé dans la production d’(in)égalités vaccinales. Ce document a été élaboré pour la SSHAP par Santiago Ripoll (IDS), Tavitha Hrynick (IDS), Ashley Ouvrier (LaSSA), Megan Schmidt-Sane (IDS), Federico Federici (UCL) et Elizabeth Storer (LSE). Il a été revu par Eloisa Franchi (Université de Pavie) et Ellen Schwartz (Conseil de santé publique de Hackney). La recherche a été financée par la British Academy COVID-19 Recovery : Fonds G7 (COVG7210038). Les recherches ont été menées à l’Institut d’études du développement (IDS), à l’Université de Sussex et au Laboratoire des sciences sociales appliquées (LaSSA). La SSHAP en assume la responsabilité.
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10

Hovav, Ran, Peggy Ozias-Akins e Scott A. Jackson. The genetics of pod-filling in peanut under water-limiting conditions. United States Department of Agriculture, gennaio 2012. http://dx.doi.org/10.32747/2012.7597923.bard.

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Pod-filling, an important yield-determining stage is strongly influenced by water stress. This is particularly true for peanut (Arachishypogaea), wherein pods are developed underground and are directly affected by the water condition. Pod-filling in peanut has a significant genetic component as well, since genotypes are considerably varied in their pod-fill (PF) and seed-fill (SF) potential. The goals of this research were to: Examine the effects of genotype, irrigation, and genotype X irrigation on PF and SF. Detect global changes in mRNA and metabolites levels that accompany PF and SF. Explore the response of the duplicate peanut pod transcriptome to drought stress. Study how entire duplicated PF regulatory processes are networked within a polyploid organism. Discover locus-specific SNP markers and map pod quality traits under different environments. The research included genotypes and segregating populations from Israel and US that are varied in PF, SF and their tolerance to water deficit. Initially, an extensive field trial was conducted to investigate the effects of genotype, irrigation, and genotype X irrigation on PF and SF. Significant irrigation and genotypic effect was observed for the two main PF related traits, "seed ratio" and "dead-end ratio", demonstrating that reduction in irrigation directly influences the developing pods as a result of low water potential. Although the Irrigation × Genotype interaction was not statistically significant, one genotype (line 53) was found to be more sensitive to low irrigation treatments. Two RNAseq studies were simultaneously conducted in IL and the USA to characterize expression changes that accompany shell ("source") and seed ("sink") biogenesis in peanut. Both studies showed that SF and PF processes are very dynamic and undergo very rapid change in the accumulation of RNA, nutrients, and oil. Some genotypes differ in transcript accumulation rates, which can explain their difference in SF and PF potential; like cvHanoch that was found to be more enriched than line 53 in processes involving the generation of metabolites and energy at the beginning of seed development. Interestingly, an opposite situation was found in pericarp development, wherein rapid cell wall maturation processes were up-regulated in line 53. Although no significant effect was found for the irrigation level on seed transcriptome in general, and particularly on subgenomic assignment (that was found almost comparable to a 1:1 for A- and B- subgenomes), more specific homoeologous expression changes associated with particular biosynthesis pathways were found. For example, some significant A- and B- biases were observed in particular parts of the oil related gene expression network and several candidate genes with potential influence on oil content and SF were further examined. Substation achievement of the current program was the development and application of new SNP detection and mapping methods for peanut. Two major efforts on this direction were performed. In IL, a GBS approach was developed to map pod quality traits on Hanoch X 53 F2/F3 generations. Although the GBS approach was found to be less effective for our genetic system, it still succeeded to find significant mapping locations for several traits like testa color (linkage A10), number of seeds/pods (A5) and pod wart resistance (B7). In the USA, a SNP array was developed and applied for peanut, which is based on whole genome re-sequencing of 20 genotypes. This chip was used to map pod quality related traits in a Tifrunner x NC3033 RIL population. It was phenotyped for three years, including a new x-ray method to phenotype seed-fill and seed density. The total map size was 1229.7 cM with 1320 markers assigned. Based on this linkage map, 21 QTLs were identified for the traits 16/64 weight, kernel percentage, seed and pod weight, double pod and pod area. Collectively, this research serves as the first fundamental effort in peanut for understanding the PF and SF components, as a whole, and as influenced by the irrigation level. Results of the proposed study will also generate information and materials that will benefit peanut breeding by facilitating selection for reduced linkage drag during introgression of disease resistance traits into elite cultivars. BARD Report - Project4540 Page 2 of 10
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