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Interleukin-17 Induces VEGFA Expression In LNCAP CellsJanuary 2019 (has links)
archives@tulane.edu / Vascular endothelial growth factor A (VEGFA) is a key contributor to the formation of
new blood vessels and angiogenesis is commonly seen in wound healing, cancer, and
inflammatory diseases. However, whether interleukin-17 (IL-17) can induce the
expression of VEGFA in prostate cancer cells remains unknown. In this study, Western
blot analysis and reverse transcription-polymerase chain reaction (RT-PCR) analysis
validated that expression of VEGFA in human prostate cancer LNCaP cells under IL-17
treatment was significantly higher than the untreated control group. The conditioned
culture medium (CM) of LNCaP cells treated with IL-17 increased tube number, tube
nodes, and tube length formed by human umbilical vein endothelial cells (HUVEC) in
tube formation assays, compared with the control CM without IL-17 treatment.
Collectively, these findings reveal that the expression of VEGFA is induced by IL-17 in
LNCaP prostate cancer cells, which leads to increased angiogenesis of HUVEC cells.
This study suggests that expression of VEGFA may be up-regulated by IL-17 in prostate
cancer to enhance tumor angiogenesis. / 1 / Benyu Li
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Regulace signalizace receptorového komplexu pro IL-17 / Regulation of IL-17 receptor complex signaling.Šemberová, Tereza January 2021 (has links)
Inflammatory immune response is essential for maintaining the defense against invading pathogens, although its aberrant activation leads to impaired self tolerance and development of autoimmune pathologies. Interleukin-17A (also known as IL-17), is a major proinflammatory cytokine, which contributes to the development and maintenance of inflammation and provides protection against several bacterial and yeast infections. However, extreme activation of IL-17 signaling leads to autoimmune pathologies. Thus, a strict regulation of IL-17 signal transduction is crucial to prevent progression of autoimmunity. Non-degradative ubiquitination is one of the main mechanisms regulating IL-17 signaling. Main E3 ubiquitin ligase within this signal transduction is TRAF6, which is also participating in several signaling pathways within the immune system. Non-degradative polyubiquitin chains created within inflammatory signaling complexes recruit signaling proteins such as IKK complex and TAK1 kinase, crucial for triggering of NF-κB and MAPKs downstream pathways. However, activation of these pathways upon IL-17 is very weak in comparison with other inflammatory stimuli, indicating a presence of a strong negative feedback loop. In this thesis, we establish the role of several regulatory molecules in IL-17 signaling....
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Étude de l'expression de l'ARNm de l'interleukine-17 dans les lavages broncho-alvéolaires des chevaux atteints du souffleDebrue, Marie January 2004 (has links)
Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.
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Promotion Of Lung Cancer By Interleukin-17Unknown Date (has links)
No description available.
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Promotion Of Lung Cancer By Interleukin-17Unknown Date (has links)
No description available.
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Promotion Of Lung Cancer By Interleukin-17Unknown Date (has links)
No description available.
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Molecular Basis of Upregulation of IL-17 in Estrogen Model of InflammationKhan, Deena 01 August 2012 (has links)
Interleukin-17 (IL-17) plays a major role in inflammation by regulating the induction of various proinflammatory genes, which aid in the recruitment and activation of neutrophils. Although IL-17 is considered to be protective in infection, overproduction of IL-17 in conditions like autoimmune diseases has been shown to aggravate these diseases and contribute to tissue injury. One of the principal focus of our laboratory is to decipher molecular mechanisms involved in inflammatory cytokine regulation and response in inflammatory disorders. To study this aspect, we employ a murine model of pro-inflammation induced by exposure to a natural immunomodulator, estrogen. In this novel study, we have comprehensively investigated the effect of estrogen on IL-17 induction, an aspect not studied thus far. We are the first to demonstrate that estrogen increases the ability of lymphocytes to secrete IL-17A, and its isoforms IL-17F, IL-17A/F. In addition to the cytokine levels, the percentages of IL-17⁺ cells are also increased by estrogen. Impressively, we found that estrogen fine tunes the balance of multiple transcription factors/signaling pathways. Estrogen upregulates IL-17 by promoting the activity and expression of positive regulators (RORγt, RORα, NF-κB, JAK-2) and decreases the activity and/or expression of negative regulators (IRF8, ETS-1). In addition, we found that estrogen epigenetically regulates IL-17 induction by miRNAs (miR-326 and miR-223). We also found that majority of IL-17 positive cells are CD8⁺ suggesting that estrogen-mediated IL-17 induction is predominantly from Tc17 cells. This is possibly due to increased proliferation of CD8⁺ cells from estrogen-treated mice, as demonstrated by CFSE cell proliferation assay. Furthermore, estrogen also enhances the ability of IL-17-target cells to release proinflammatory molecules when exposed to IL-17. Together, this is the first study to comprehensively show that estrogen calibrates transcription factors and miRNAs to enhance IL-17 induction and promote IL-17 response. This dissertation work will provide a platform to continue further research in estrogen modulation of IL-17 in inflammation and disease conditions. / Ph. D.
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Einfluss von Antipsychotika auf die Zytokinproduktion in-vitroSchönherr, Jeremias 06 June 2016 (has links) (PDF)
Diese Arbeit beschreibt Ergebnisse einer in-vitro Untersuchung der Antipsychotika
Chlorpromazin, Haloperidol, Clozapin, N-Desmethylclozapin und Quetiapin bezüglich ihrer
Wirkung auf die Zytokinproduktion. Dafür wurde Vollblut von gesunden Probandinnen invitro
mit dem Immunmodulator Toxic-Shock-Syndrome-Toxin-1 (TSST-1) stimuliert. Dabei
wurden die Konzentrationen der Zytokine Interleukin (IL)-1ß, IL-2, IL-4, IL-6, IL-17 und
Tumornekrosefaktor-α (TNF-α) im unstimulierten Blut und im stimulierten Blut, jeweils mit
und ohne Zusatz der Antipsychotika gemessen.
Es zeigte sich, dass TSST-1 eine signifikante Stimulation der Produktion aller getesteten
Zytokine bewirkte und dass es über diese Stimulation mit TSST-1 hinaus zu einer Erhöhung
von IL-17 unter allen getesteten Antipsychotika kam.
Aufgrund dieser Ergebnisse ist es denkbar, dass Antipsychotika, in Ergänzung zu ihrer
Wirkung an Dopaminrezeptoren, auch über diese immunologische Eigenschaft Wirkungen
und Nebenwirkungen entfalten können. Weiterhin könnte die IL-17-Produktion ein
Biomarker in der Behandlung mit Antipsychotika sein, der wiederum zur individuellen
Vorhersage von Wirkungen und Nebenwirkungen beitragen könnte.
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Avaliação da ação da IL-17 em macrófagos peritoneais murinosMartins, Lohane Suzart 25 July 2014 (has links)
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Previous issue date: 2014-07-25 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES / L. (L.) amazonensis is one of the species that cause American tegumentary leishmaniasis. Resistance to Leishmania infection is associated with Th1 lymphocytes, which produce IFN-γ and activate macrophages and promote the death of the parasites. However, during the infection, other T cells subtypes can develop, such as the Th17 subtype, which produce IL-17. The role of IL-17 is known in inflammatory diseases and infections with extracellular pathogens, and its function is associated to the migration and activation of neutrophils. In Leishmania infection, it is not clear whether this cytokine would influence the activation of a phenotype that controls infection. Aim: To assess whether IL-17 interferes with activation of murine macrophages and with their Leishmania amazonensis leishmanicidal. Methods: Thyoglycolate-elicited peritoneal macrophages from BALB/c or C57BL/6 mice were primed with IL-17, IFN-γ or IL-4, activated or not with lipopolysaccharide (LPS) and infected with L. (L.) amazonensis promastigotes. Culture supernatants were harvested 48 h after the stimulus to assess nitric oxide (NO) and IL-12p40 production. The cells were used to determine the phagocytic, leishmanicidal and arginase activity. Results: Macrophages from BALB/c and C57BL/6 mice stimulated with IL-17 and LPS produced IL-10 and increased arginase activity. IL-17 was not able to induce NO production by these cells, but promoted a small increase in IL-12p40 secretion by C57BL/6 mice macrophages. IL-17 favored the proliferation of Leishmania in macrophages from BALB/c mice, but not in C57BL/6 mice. A synergism was observed between IL-17 and IL-4 that increased IL-10 production and arginase activity in macrophages from BALB/c mice. In macrophages from C57BL/6 mice, however, a synergism was observed between IL-17 and IFN-γ in the stimulation of NO production. Conclusion: These results suggest that IL-17 may participate in the activation of macrophages toward either phenotype depending on the mouse strain. The finding that IL-17 impairs the control of L. (L.) amazonensis in BALB/c mice was not observed in C57BL/6 mice. IL-10 production in macrophages stimulated with IL-17 suggests a regulatory role of this last cytokine. / A L. (L.) amazonensis é uma das espécies que causam a leishmaniose tegumentar americana. A resistência à infecção é associada à linfócitos Th1, os quais produzem IFN-γ que ativam macrófagos e promovem a morte do parasito. No entanto, durante a infecção, há o desenvolvimento de outros perfis de linfócitos, como o Th17, que produz IL-17. O papel da IL-17 é bem descrito em doenças inflamatórias e infecções por patógenos extracelulares, sendo que sua função está relacionada com a quimiotaxia e ativação de neutrófilos. Quanto à infecções por patógenos intracelulares, como a leishmânia, não está claro se esta citocina poderia agir interferindo no perfil dos macrófagos e, consequentemente, no controle da doença. Objetivo: avaliar se a IL-17 é capaz de influenciar na ativação dos macrófagos e nos mecanismos leishmanicidas de macrófagos murinos infectados com L. (L.) amazonensis. Métodos: macrófagos peritoneais de camundongos BALB/c e C57BL/6 foram estimulados com IFN-γ, IL-4 ou IL-17, ativados ou não com LPS e infectados com promastigotas de L. (L.) amazonensis. O sobrenadante foi utilizado para avaliar produção de NO, IL-12p40 e IL-10 e as células remanescentes usadas para avaliar a atividade de arginase, a atividade fagocítica e leishmanicida. Resultados: macrófagos de camundongos BALB/c e C57Bl/6 estimulados com IL-17 e LPS produziram IL-10 e aumentaram a atividade de arginase. A IL-17 não foi capaz de induzir a produção de NO pelos macrófagos, mas promoveu um pequeno aumento da produção de IL-12p40 em macrófagos de C57BL/6. A IL-17 favoreceu a proliferação da L. (L.) amazonensis em macrófagos de camundongos BALB/c, mas não nos de camundongos C57BL/6. Observou-se um sinergismo entre IL-17 e IL-4 na produção de IL-10 e a atividade de arginase em macrófagos de camundongos BALB/c. Em macrófagos de camundongos C57BL/6, por sua vez, foi observado sinergismo entre IL-17 e IFN-γ para a produção de NO. Conclusão: A IL-17 pode estar relacionada tanto com a ativação clássica de macrófago quanto com sua ativação alternativa. Porém, a morte da leishmânia é prejudicada em macrófagos de BALB/c estimulados com IL-17. A indução da produção de IL-10 em macrófagos estimulados com IL-17 sugere um potencial regulador desta última citocina.
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IL-17/Th17 au cours de l'inflammation chronique : ciblage des interactions cellulaires / IL-17/Th17 during chronic inflammation : targeting of cellular interactionsNoack, Mélissa 22 September 2016 (has links)
Lors de l'inflammation chronique, les cellules immunitaires, dont les lymphocytes Th17 (LTh17), migrent au niveau du site inflammatoire et interagissent avec les cellules mésenchymateuses locales. Dans deux contextes inflammatoires, la polyarthrite rhumatoïde (PR) et le psoriasis (Pso), le but de ce travail a été d'étudier le rôle de ces interactions cellulaires sur la production de cytokines pro-inflammatoires, et principalement l'IL-17, et d'identifier les mécanismes impliqués.L'utilisation d'un système de co-culture entre cellules mésenchymateuses (synoviocytes PR ou fibroblastes de peau Pso) et cellules mononuclées du sang périphérique mimant la situation in vivo, a permis d'étudier l'effet de ces interactions. Le contact cellulaire suffisait à l'induction de la sécrétion d'IL-6, d'IL-8 ou d'IL-1ß. En revanche, la forte sécrétion d'IL-17 nécessitait le contact cellulaire mais également l'activation du TCR. L'inhibition de la podoplanine (pdpn), molécule d'interaction exprimée par différents types cellulaires (cellules mésenchymateuses mais également LTh17), diminuait significativement la production d'IL-17. Toutefois, cette inhibition n'était pas totale, c'est pourquoi une étude en collaboration est en cours afin d'identifier d'autres molécules impliquées.Cette étude a donc montré que les interactions entre cellules mésenchymateuses et cellules immunitaires jouent un rôle majeur dans la sécrétion de cytokines pro-inflammatoires, notamment dans la forte production d'IL-17. La podoplanine semble largement impliquée dans ce mécanisme, ce qui en fait une cible thérapeutique potentielle pour bloquer l'activité Th17 lors de l'inflammation chronique / During chronic inflammation, immune cells, including Th17 lymphocytes, migrate to the inflammatory site and interact with the local mesenchymal cells. In two inflammatory contexts, rheumatoid arthritis (RA) and psoriasis (Pso), the aim of this work was to study the effect of cellular interactions on pro-inflammatory cytokine production, with a focus on IL-17, and to identify the involved mechanisms. Using a co-culture system between mesenchymal cells (RA synoviocytes or Pso skin fibroblasts) and peripheral blood mononuclear cells mimicking the in vivo situation, allowed studying the effect of these cell interactions. The cell contact alone was sufficient to induce IL-6, IL-8 and IL-1ß secretion. On the contrary, the heightened IL-17 production required the cell contact and the TCR activation. The inhibition of the podoplanin (pdpn), interaction molecule expressed by different cell types (including mesenchymal cells but also Th17 lymphocytes), decreased significantly the IL-17 production. Nevertheless, this inhibition was only partial, which leads to a collaboration in order to identify other involved molecules. In conclusion, this study showed that cell interactions between mesenchymal cells and immune cells play a major role in the pro-inflammatory cytokine production, leading to a heightened IL-17 secretion. The podoplanin molecule seems play a crucial role in this mechanism, and thus pdpn could be a potential therapeutic target to block Th17 cell activity during chronic inflammation
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