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Dissertations / Theses on the topic 'Interleukin-4'

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Published: 4 June 2021
Last updated: 15 June 2025

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1

Silfverswärd, Carl-Johan. "Effects of Interleukin-4 and Interleukin-13 on Bone." Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8414.

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<p>Cytokines play important roles in bone metabolism, participating in the complex interplay necessary for normal bone formation and turnover. The aim of the present thesis was to investigate the effects of two anti-inflammatory cytokines, interleukin-4 (IL-4) and interleukin-13 (IL-13) on bone. </p><p>Influence of pro- and anti-inflammatory cytokines on interleukin-6 (IL-6) formation in cultured human osteoblasts (hOBs) was investigated. IL-4 and IL-13 as well as interleukin-1 (IL-1) and tumour necrosis factor alpha and beta (TNF-α/β) stimulated IL-6 secretion in hOBs. Also, IL-4 and IL-13 synergistically potentiated the effect of IL-1 and TNFs on IL-6 secretion. </p><p>Effects of IL-4 and IL-13 on markers of osteoblastic activity in hOBs were investigated. IL-4 and IL-13 induced a dose-dependent increase in the formation of alkaline phosphatase (ALP) and pro-collagen type I carboxy-peptide (PICP) together with enhanced mineralization rate in hOBs. Formation of osteocalcin (OC) was unaffected. </p><p>The mechanism behind inhibited proliferation by IL-4 and IL-13 in hOBs was investigated. IL-4 and IL-13 caused a dose-dependent increase in DNA-fragmentation together with escalating Caspase-3 activity in hOBs, reflecting induced apoptosis. Osteoblast apoptosis was also confirmed by TNF-α, dexamethasone and by serum starvation.</p><p>The skeletal phenotype of IL-13<sup>-/-</sup>, IL-4<sup>-/-</sup>IL-13<sup>-/-</sup> and WT mice was compared. An altered cortical bone mass was detected in adult male IL-4<sup>-/-</sup>IL-13<sup>-/-</sup> mice. They displayed a reduction in cortical bone mineral content (BMC) secondary to reduced cortical thickness. Mechanical strength of the cortical bone was reduced in level with the reduction detected in BMC. Trabecular bone mineral density (tvBMD) was unaffected. </p><p>Callus formation in IL-4<sup>-/-</sup>IL-13<sup>-/-</sup> and WT male mice was compared. No differences were found concerning radiological healing, biomechanical properties, callus parameters or histology. Heterotopic bone formation in IL-4<sup>-/-</sup>IL-13<sup>-/-</sup> and WT mice was compared using DXBM implants. No differences were found concerning mineralization of implants. Immuno-histology showed inhibition of autonomic nerves and lack of implant vascularization in IL-4<sup>-/-</sup>IL-13<sup>-/-</sup> mice. </p><p>In summery, the two anti-inflammatory cytokines IL-4 and IL-13 influence osteoblast activity and apoptosis <i>in vitro</i>. They also selectively influence cortical bone formation <i>in vivo</i>. These findings suggest a role for IL-4 and IL-13 in osteoblast differentiation, in bone metabolism and in bone formation. </p>
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2

Silfverswärd, Carl-Johan. "Effects of Interleukin-4 and Interleukin-13 on Bone /." Uppsala : Acta Universitatis Upsaliensis, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8414.

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3

Parker, Ruth E. "The rat interleukin-4 receptor." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318893.

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4

Traub, Benno [Verfasser]. "Einfluss der Interleukin-4-Interleukin-4-Rezeptor-Kaskade auf den malignen Phänotyp kultivierter Pankreaskarzinomzellen / Benno Traub." Ulm : Universität Ulm, 2017. http://d-nb.info/1140118161/34.

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5

Piehler, Daniel. "The inflammatory response against Cryptococcus neoformans is regulated by eosinophilic granulocytes and the interleukin-4/interleukin-4 receptor axis." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-78248.

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Cytokines play an important regulatory role during immune responses against pathogens. The outcome of an induced cytokine pattern is determined by many factors. It strongly depends on the nature of the pathogen and the host’s ability to control the quality and strength of cytokine signals. In pulmonary infection with Cryptococcus neoformans T helper (Th) 1 and Th17 cell subsets and their associated cytokines confer protection, whereas a Th2-biased response with production of interleukin (IL) -4 confers susceptibility. Since inappropriate Th responses often lead to death in immunosuppressed human patients, especially HIV-1 infected patients, this work aimed to elucidate mechanisms of Th2 induction and regulation by assessing the Th2 hallmark cytokine IL-4 in an experimental model of cryptococcosis. Therefore, a kinetic study of IL-4 expression during 70 days after intranasal infection was performed in susceptible mice. The analyses included characterization of pulmonary leukocytes and Th cell cytokine profiling. IL-4 profiling revealed Cryptococcus-specific IL-4 production not before six weeks after infection. This unexpected finding was further validated by equal results observed in a kinetic study done in IL-4 reporter mice. These mice express a green fluorescent protein simultaneously to IL-4 expression in the same cell and this protein can be detected by flow cytometry. Two cellular sources of IL-4 were identified: Th2 cells were found as expected, but also, as shown for the first time, eosinophilic granulocytes could be demonstrated to secrete IL-4. Next, the influence of eosinophils on pulmonary inflammation and disease development was investigated using ΔdblGATA-1 mice constitutively devoid of eosinophilic granulocytes. Experiments with infected ΔdblGATA-1 mice revealed novel regulatory functions of eosinophils in cryptococcosis. In the absence of eosinophils pulmonary Th cell recruitment was significantly diminished. In addition, Th2 polarization was reduced in ΔdblGATA-1 mice as shown by reduced numbers of Th2 cells expressing the Th2-related surface marker T1/ST2 and reduced albeit not absent IL-4 production by Th cells. In addition to reduced IL-4 production, in the absence of eosinophils Th cells with enhanced interferon-γ and IL-17 production were observed. However, control of pulmonary fungal growth was only slightly enhanced in the absence of eosinophils and dissemination of cryptococci to the brain was unaltered. This may be related to the shared IL-4 production by not only eosinophils but also Th2 cells. Blocking more than one cellular source of IL-4 could be required to prevent immunopathology. To test the hypothesis of gradual IL-4-dependent immunopathology, experiments were conducted using mice expressing only one allele of the IL-4receptor (R) alpha (α) chain (+/-) instead of two (+/+). Indeed, mono-allelic expression of the IL-4Rα resulted in an intermediate expression of the IL-4R on the surface of myeloid and lymphoid cells indicating a gene-dosage effect for IL-4R expression. Infected IL-4Rα+/- mice displayed reduced susceptibility as compared with IL-4Rα+/+ mice, and IL-4Rα-/- mice completely lacking IL-4R expression were found to be protected with survival for the complete time period of the experiment (i.e. up to 275 days). Reduced susceptibility found in infected IL-4Rα+/- mice was associated with decreased serum levels of immunoglobulin E, reduced mucus production by airway epithelia, attenuation of airway hyper-reactivity, and reduced formation of alternatively activated macrophages in lung parenchyma – pathophysiological features, which are typically found in experimental models of asthma but also in asthma of humans and animals. Since no up-regulation of IL-4R by the infection with Cryptococcus neoformans was found, the experimental pulmonary infection model used appears to be a very sensitive low-level IL-4 system. This work highlights the outstanding role of IL-4 and its different cellular sources as well as its receptor in cryptococcosis and provides novel insights into pathogenesis. Moreover, a cellular (i.e. eosinophils) and a molecular (i.e. IL-4R) target for treatment of this mycosis and possibly of asthma is provided.
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6

McKenzie, Grahame James. "Analysis of interleukin-13 and interleukin-4 function using gene targeting." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624953.

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7

Moga, Simona. "Bestimmung der Zytokine Interleukin-1α, Interleukin-1β, Interleukin-2, Interleukin-3 und Interleukin-4 im Vaginalsekret bei Frauen mit Bakterieller Dysbiose". Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-75888.

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8

Clarke, Christopher Jeremy Paul. "Molecular mechanisms of the anti-inflammatory cytokines interleukin-4 and interleukin-10." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285172.

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9

Alvi, Azra Johanna. "Heterogeneity of lymphokine-activated killer cells: Role of interleukin-2 and interleukin-4." Thesis, University of Ottawa (Canada), 1990. http://hdl.handle.net/10393/5579.

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Our main objective was to determine if the Lymphokine Activated Killer cells (LAK) activity is restricted to Natural Killer (NK) cells or if it is also detectable in T cell subsets, especially in CD3+ T cells that are also negative for CD4 and CD8 cell surface markers. We were able to obtain highly purified subsets of NK cells, helper/inducer (CD3+4+8$-$), suppressor/cytotoxic (CD3+4$-$8+) and double negative (CD3+4$-$8$-$) T cells. The double negative T cells are now known to be a subset of $\gamma\delta$-T cells. Highly purified subsets were obtained using antibody (sheep anti-mouse IgG) coated magnetic particles and monoclonal antibodies. The purified subsets were tested for LAK activity against a standard target cell (K562), a NK resistant/LAK sensitive target cell (HTB 38), and a NK/LAK resistant target cell. We found NK cells develop LAK activity after IL-2 stimulation and that two T cell subsets (cytotoxic/suppressor and double negative) consistently showed LAK activity (3 experiments). The helper/inducer subset showed LAK activity in 2 of 3 experiments. Interleukin 4 had an inhibitory effect on the proliferative activity of IL-2 stimulated T cells and was not used in the LAK experiments. In conclusion we have found that the LAK function is a property of an heterogeneous group of lymphocyte subsets that includes NK cells and T cell subsets. (Abstract shortened by UMI.)
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10

Schardt, Victor. "Vergleichende Untersuchungen zur Hefepilzbesiedelung von Mundhöhle und Vagina und Bestimmung von Interleukin-4, Interleukin-10 und Interleukin-12." Diss., lmu, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-155152.

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11

Braun, Philipp [Verfasser]. "Expression von Interleukin-4, Interleukin-4 Rezeptor, Interleukin-13 und Interleukin-13 Rezeptor in gastrointestinalen Tumoren und deren Rolle als prognostischer Faktor - eine retrospektive Untersuchung am Tumorgewebe von 454 Patienten / Philipp Braun." Ulm : Universität Ulm. Medizinische Fakultät, 2013. http://d-nb.info/1035699753/34.

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12

Khan, Shamila. "Therapeutic effect of Interleukin-4 and Interleukin-1 Receptor Antagonist in Actinobacillus pleuropneumoniae challenged pigs." Thesis, The University of Sydney, 2005. http://hdl.handle.net/2123/625.

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Immunological stressors, in the form of clinical and sub-clinical disease are currently controlled using both prophylactic antibiotics in-feed, and therapeutic antibiotic treatment. Respiratory disease, primarily Actinobacillus pleuropneumoniae (App) infection, is recognised as a major factor causing reduced productivity in pigs. This thesis reports investigations into the use of novel immunomodulators in particular Interleukin 4 (IL-4) and Interleukin 1 receptor antagonist (IL-1ra) as alternatives to antibiotics to treat App infection. Immunological and molecular biological assays were used to investigate and accumulate data. An in vitro study undertaken to find potential anti-inflammatory substances, revealed that Interleukin 8 (IL-8) mRNA production stimulated by PMA or LPS in whole pigs' blood was suppressed by IL-4. IL-1ra also suppressed stimulated IL-8 mRNA production by heat killed App bacteria (KB) in vitro. An acute LPS challenge in pigs in vivo however, showed no variation in illness or weight loss between pigs treated prophylactically with anti-inflammatory substance (IL-4 and IL-1ra) and saline treated pigs. The use of plasmids as a delivery system for anti-inflammatory substance did not show promise since it did not enhance growth or prolong the expression of the substances in the pigs. However, in the chronic App challenge model IL-4 and IL-1ra administered prophylactically in vivo showed an ability to improve growth. The therapeutic administration of IL-4 and IL-1ra to App challenged pigs showed no difference in pigs' growth, regardless of the treatment or control administered. To conclude, IL-4 and IL-1ra showed promise when administered prophylactically and improved growth and abrogated disease under conditions of App challenge. However when IL-4 and IL-1ra where administered therapeutically they did not perform as well. Moreover these compounds have potential as a commercial application to reduce the growth reduction caused by disease such as App.
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13

Cleaver, Catherine Sarah. "The role of interleukin-4 and interleukin-13 in the prevention of cartilage breakdown." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327238.

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14

Lerch, Steffen [Verfasser]. "Interleukin-4 receptor pathway in neurons / Steffen Lerch." Mainz : Universitätsbibliothek Mainz, 2018. http://d-nb.info/1173807683/34.

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15

Chakraborty, Rikhia. "Homeostatic Regulation of Interleukin-4-Mediated Cell Signaling." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1258663290.

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16

Azbil, Tatiana. "Nachweis von Candida-Spezies und Bestimmung der Zytokine Interleukin-1 beta, Interleukin-1ra, Interleukin-4, Interleukin-6, Interleukin-8, Interleukin-10 und Interleukin-12 im Vaginalsekret und im Serum bei Schwangeren in Relation zum Gestationsalter." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57576.

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17

Khan, Shamila. "Therapeutic effect of Interlenkin-4 and Interleukin-1 receptor antagonist in Actinobacillus pleuropneumoniae challenged pigs." University of Sydney. Anatomy and Pathology, 2005. http://hdl.handle.net/2123/625.

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Immunological stressors, in the form of clinical and sub-clinical disease are currently controlled using both prophylactic antibiotics in-feed, and therapeutic antibiotic treatment. Respiratory disease, primarily Actinobacillus pleuropneumoniae (App) infection, is recognised as a major factor causing reduced productivity in pigs. This thesis reports investigations into the use of novel immunomodulators in particular Interleukin 4 (IL-4) and Interleukin 1 receptor antagonist (IL-1ra) as alternatives to antibiotics to treat App infection. Immunological and molecular biological assays were used to investigate and accumulate data. An in vitro study undertaken to find potential anti-inflammatory substances, revealed that Interleukin 8 (IL-8) mRNA production stimulated by PMA or LPS in whole pigs' blood was suppressed by IL-4. IL-1ra also suppressed stimulated IL-8 mRNA production by heat killed App bacteria (KB) in vitro. An acute LPS challenge in pigs in vivo however, showed no variation in illness or weight loss between pigs treated prophylactically with anti-inflammatory substance (IL-4 and IL-1ra) and saline treated pigs. The use of plasmids as a delivery system for anti-inflammatory substance did not show promise since it did not enhance growth or prolong the expression of the substances in the pigs. However, in the chronic App challenge model IL-4 and IL-1ra administered prophylactically in vivo showed an ability to improve growth. The therapeutic administration of IL-4 and IL-1ra to App challenged pigs showed no difference in pigs' growth, regardless of the treatment or control administered. To conclude, IL-4 and IL-1ra showed promise when administered prophylactically and improved growth and abrogated disease under conditions of App challenge. However when IL-4 and IL-1ra where administered therapeutically they did not perform as well. Moreover these compounds have potential as a commercial application to reduce the growth reduction caused by disease such as App.
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18

Kampshoff, Jörg. "Die Wirkung der Interleukine 4, 10 und 13 auf die Koinkubation von Endothelzellen und mononukleären Zellen, gemessen an der Freisetzung von PDGF, Interleukin-1-[beta] [Interleukin-1-beta] und Interleukin-6." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972057684.

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19

Kraich, Michael. "Strukturelle und funktionelle Untersuchungen der Interaktion zwischen Ligand und Rezeptor im Interleukin-4- und Interleukin-13-System." Doctoral thesis, kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2008/2765/.

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20

Lasoudris, Fanette. "Immunosuppression associée à l’enzyme interleukine-4 induced gene 1 (IL4I1) : régulation de l’expression dans les cellules humaines et rôle dans l’échappement tumoral à la réponse immune dans un modèle murin." Thesis, Paris Est, 2011. http://www.theses.fr/2011PEST0089/document.

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La protéine IL4I1 est une enzyme sécrétée dont l’activité L-amino acide oxydase vis-à-visde la phénylalanine inhibe la prolifération des lymphocytes T in vitro (Boulland et al, Blood 2007).Comme d’autres enzymes immunosuppressives, elle est exprimée dans les tumeurs au niveau descellules myéloïdes et/ou des cellules tumorales (Carbonnelle-Puscian et al, Leukemia 2009). Le but decette thèse a été de caractériser les conditions d’expression d’IL4I1 et de comprendre son rôle dans lecancer.Nous avons montré que les macrophages et les cellules dendritiques représentent la principalesource d’IL4I1 in vitro et dans des lésions inflammatoires chroniques. L’expression d’IL4I1 dans lesphagocytes mononucléés est induite par les interférons ou les ligands de TLR, activant respectivementSTAT1 et NF-kB, tandis que les lymphocytes B expriment des niveaux nettement plus faibles d’IL4I1sous le contrôle de la voie IL-4/STAT6 et de la voie CD40/NFkB. L’expression d’IL4I1 par des cellulesmonocytaires inhibe la production de cytokines Th1 et pourrait donc contribuer à la régulation del’inflammation Th1 in vivo.Dans un modèle murin de cancer, l’expression d’IL4I1 facilite le développement tumoral endiminuant la réponse T cytotoxique spécifique de la tumeur. Ceci est observé à des niveaux d’activitéIL4I1 proches de ceux mesurés dans des tumeurs humaines, suggérant qu’IL4I1 puisse contribuer àl’échappement des tumeurs au système immunitaire chez l’homme. Nous avons développé plusieursmutants d’IL4I1, afin d’évaluer l’impact de l’activité enzymatique versus celui de l’éventuelle liaison del’enzyme à un récepteur, dans l’effet protumoral observé. Un de ces mutants est actuellementdisponible pour une étude chez la souris.Nos résultats installent définitivement IL4I1 dans le panorama des enzymesimmunosuppressives associées au cancer et ouvrent la voie au développement d’inhibiteursspécifiques comme outils thérapeutiques<br>The IL4I1 protein is a secreted L-amino acid oxidase, which inhibits T cell proliferationthrough phenylalanine degradation in vitro (Boulland et al, Blood 2007). Similar to previously describedimmunosuppressive enzymes, IL4I1 is expressed in cancer by myeloid cells and/or tumor cells(Carbonnelle-Puscian et al, Leukemia 2009). The aim of this work was to characterize the cells andstimuli associated with IL4I1 expression and to decipher its role in cancer.We showed that macrophages and dendritic cells are the main source of IL4I1 in vitro and inchronic inflammatory lesions. IL4I1 expression in mononuclear phagocytes is induced by interferons orTLR ligands, which act through STAT1 and NFkB respectively. Conversely, B cells express dramaticallylower levels of IL4I1 under the control of IL-4/STAT6 and CD40/NFkB. IL4I1 expression by monocyticcells inhibits the production of Th1 cytokines and may thus contribute to Th1 inflammation control invivo.In a murine model of cancer, IL4I1 expression facilitates tumor development by depressing thetumor specific cytotoxic T cell response. This is observed for IL4I1 activity levels in the range of thosemeasured in human tumors, suggesting that IL4I1 may contribute to tumor immune escape in humans.We developed several IL4I1 mutants to discriminate the role of the enzymatic activity versus the bindingto a putative cell surface receptor in the protumor effect observed. One of these mutants is currentlyavailable for in vivo testing.Our results definitively establish IL4I1 in the family of immunosuppressive enzymes associatedwith cancer and pave the way for the development of specific inhibitors as therapeutic tools
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21

Blalock, Emily L. "Roles of TH2 and TH17 CD4+ T-Helper Cell Cytokines in the Pathogenesis of Experiemental Cytomegalovirus Retinitis." Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/biology_diss/122.

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Human cytomegalovirus (HCMV) is a betaherpesvirus that infects up to 80% of the population worldwide, and establishes latency in monocytes and bone marrow cells. Reactivated HCMV can become an opportunistic pathogen in individuals who are immunocompromised, such as those with acquired immunodeficiency syndrome (AIDS). HCMV infection of AIDS patients causes a sight-threatening retinitis that leads to vision loss and blindness in up to 46% of this population without antiretroviral treatment. Because untreated HIV-infected individuals exhibit the loss of cell-mediated immunity and alterations in CD4+ T-helper (Th) cell cytokines, including elevation of interleukin-4 (IL-4), IL-10, and IL-17, we sought to test the hypothesis that these cytokines play key roles in governing the susceptibility to AIDS-related HCMV retinitis. This hypothesis was tested utilizing a clinically relevant mouse model of experimental murine cytomegalovirus (MCMV) retinitis that occurs in C57BL/6 mice immunosuppressed by mouse retroviruses (MAIDS). Studies revealed that MAIDS progression was associated with increased levels of IL-4 and IL-10, cytokines whose production has been associated with diminished CD8+ T-cell-mediated immunity during HIV infection. However, MCMV–infected eyes of retinitis-susceptible IL-4-/- or IL-10-/- MAIDS mice exhibited frequency and severity of retinitis and viral titers equivalent to MCMV-infected eyes of wild-type MAIDS animals. These studies indicated that neither IL-4 nor IL-10 alone play key roles in increased susceptibility to MCMV retinitis. In comparison, IL-17, an inflammatory cytokine associated with the ocular autoimmune disease uveitis, was systemically increased during the progression of MAIDS, but MCMV-infected eyes of retinitis-susceptible MAIDS mice exhibited a significant reduction in IL-17. These findings suggested that IL-17 plays no direct role in the pathogenesis of experimental MCMV retinitis. However, these results also suggested the remarkable possibility that MCMV downregulates IL-17 production, a hypothesis supported by the observation that systemic MCMV infection of healthy and MAIDS mice resulted in the downregulation of IL-17. Mechanistic studies revealed that knockdown of IL-10 resulted in a partial recovery IL-17 levels during MCMV infection. We conclude that MCMV-induced IL-17 downregulation occurs via the stimulation of IL-10 and the suppressor of cytokine signaling (SOCS)-3. Taken together, our results add new information to the immunobiology of HCMV and to our basic understanding of the pathogenesis of AIDS-related HCMV retinitis.
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22

Pandey, Shubham. "Identification of Interleukin 4 - CXCL12 supportive loop in follicular lymphoma." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B031/document.

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Le lymphome folliculaire (FL) est le lymphome B indolent le plus fréquent. Outre des altérations géniques récurrentes, le micro-environnement tumoral, et notamment les cellules stromales lymphoides,joue un rôle majeur dans le développement de ce cancer. Cependant, la caractérisation in-situ des cellules stromales lymphoïdes chez l'homme tout comme les facteurs menant à la polarisation du stroma en un stroma protumoral ont été peu étudiés. Dans cette thèse, nous avons montré, que les cellules stromales présentes dans les ganglions et la moelle osseuse envahis des patients atteints de FL surexpriment fortement la chimiokine CXCL12. Nous avons ensuite tenté de comprendre les mécanismes responsables de cette induction. Alors que les cellules B tumorales induisent une surexpression de la chimiokine CCL2 dans les cellules stromales de façon dépendante de leur synthèse de TNF, elles ne contribuent pas à l'induction de CXCL12. A l'inverse, le principal compartiment TCD4 impliqué dans la croissance tumorale du FL, les cellules T follicular helper (TFH), augmentent l'expression de CXCL12 dans les cellules stromales. Le taux d'IL-4, la principale cytokine produite par les TFH de FL, est d'ailleurs corrélé à celui de CXCL12 au sein de ma niche tumorale du FL. De plus, à l’aide d'un modèle de différenciation en stroma lymphoide, nous avons démontré que l’IL4 induit l’expression de CXCL12 par les cellules stromale in vitro. Cette production est augmentée quand les cellules stromales sont déjà engagées vers la voie de différentiation lymphoide par un traitement TNF/LT qui favorise l'activation de STAT6 par l'IL-4. Nous avons validé ces résultats dans un modèle de formation d'organe lymphoide ectopique chez la souris. Enfin, CXCL12 induit la migration et l'adhésion au stroma des B de FL via l'activation de cascades de signalisations qui peuvent être abrogées par l'utilisation d'un inhibiteur de Btk utilisé en clinique, l'Ibrutinib. Ces résultats sont en faveur de l'intérêt de considérer la boucle IL-4/CXCL12 pour développer de nouvelles stratégies thérapeutiques dans cette pathologie constamment fatale<br>Follicular lymphoma (FL) is the most frequent indolent B-cell lymphoma. Beside recurrent genetic alterations, tumor microenvironment, including lymphoid stromal cells, has been shown to play a key role in FL development. However, in situ characterization of lymphoid stromal cells is still lacking in humans and there are very few studies focusing on the factors that could lead to stroma polarization in normal and pathological context. In this thesis, we showed first that in FL, lymph node (LN) and bone marrow (BM) infiltrating stromal cells highly express the chemokine CXCL12. We next focused on the mechanisms underlying this upregulation. Interestingly, whereas malignant FL B cells induced overexpression of CCL2 in stromal cells in a TNF-dependent manner, they did not contribute to CXCL12 induction. Conversely, FL-infiltrating follicular helper T cells (FL-TFH), the key FL-supportive T-cell subset could trigger CXCL12 expression in stromal cells. IL-4 is the main FL-TFH-derived cytokine and showed a positive correlation with CXCL12 expression inside FL cell niches. Moreover, based on our in vitro lymphoid stroma differentiation model, we demonstrated that IL-4 promoted CXCL12 expression in stromal cells, together with a phenotype close to that identified in situ within FL cell niche. Such IL4 dependent CXCL12 regulation is more pronounced in stromal cells already committed towards lymphoid stromal cells by a prestimulation by TNF/LT in association with an increased STAT6 activation. These data were validated in a model of ectopic lymphoid organ formation in mice. Finally, CXCL12 induced FL B-cell migration, and adhesion to stromal cells through the activation of a signaling pathway that could be abrogated by the Btk inhibitor Ibrutinib. These data argue for considering IL-4/CXCL12 axis as a potential therapeutic target to disrupt FL protective cell niche in this still fatal malignancy
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23

Arnhold, Markus [Verfasser]. "Einfluss von Interleukin-4 auf die pulmonale Sensibilisierung / Markus Arnhold." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2013. http://d-nb.info/1031271791/34.

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24

Hühner, Laura [Verfasser], and Björn [Akademischer Betreuer] Spittau. "Untersuchungen zur Interleukin-4-vermittelten Protektion dopaminerger Neuronen in vitro." Freiburg : Universität, 2020. http://d-nb.info/1220225592/34.

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25

Schardt, Victor [Verfasser], and Ernst Rainer [Akademischer Betreuer] Weissenbacher. "Vergleichende Untersuchungen zur Hefepilzbesiedelung von Mundhöhle und Vagina und Bestimmung von Interleukin-4, Interleukin-10 und Interleukin-12 / Victor Schardt. Betreuer: Ernst Rainer Weissenbacher." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1032862645/34.

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26

Haake, Markus. "Stat6-vermittelte-Genregulation in eukaryontischen Zellen." Doctoral thesis, [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=964213702.

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27

Jones, Lucy Helen. "Alternative activation of dendritic cells." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8284.

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The alternative activation of macrophage populations by Interleukin-4 (IL-4) is well characterised. Alternatively activated macrophages (AAM) express high levels of the arginine converting enzyme arginase-1, and express a plethora of IL-4 driven molecules including the resistin like molecule alpha (RELMα) and the chitinase like molecule Ym1/2. Dendritic cells (DCs) are the professional antigen presenting cells (APC) of the immune system, responsible for the detection of invading pathogens, secretion of cytokines and the subsequent activation of T-cells. This thesis addresses whether IL-4 is able to ‘alternatively activate’ DCs both in vitro and in vivo, in a manner similar to that of AAM. The impact of IL-4 on DC and macrophage activation was compared and contrasted, and it was confirmed for the first time that IL-4 can alternatively activate DCs, inducing high level expression of a range of alternative activation associated markers including RELMα, Ym1/2, CCL24 and dectin-1, with the exception of arginase. DCs were significantly more capable at the in vivo priming of T-cell responses in the context of both Th1 and Th2 polarising antigens than similarly exposed macrophages, confirming their superior capacity as APC. The requirements for DC IL-4Rα expression were assessed, and IL-4 responsiveness was found to be required for the optimal induction of Th1 responses. Conversely, selective loss of only one facet of the IL-4 response, namely RELMα expression, limited the ability of IL-4 exposed DCs to induce the regulatory cytokine IL-10 both in vitro and in vivo. Furthermore, alternatively activated DCs (AADCs) were found in the spleen following 8 weeks of infection with the parasitic trematode Schistosoma mansoni, highlighting a role for DC alternative activation in a disease setting. IL-4 was shown to induce expression of the vitamin A converting enzyme aldehyde dehydrogenase, and the product of such activity, retinoic acid (RA), was found to promote the expression of RELMα in IL-4 exposed DCs. Aldehyde dehydrogenase activity was found to inversely correlate with DC expression of Ym1/2 and inhibition of RA signalling limited IL-4 driven RELMα and promoted Ym1/2.
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Banks, Emma M. S. "Mast cell secretory function in vitro : the effects of interleukin-4." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295824.

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29

Deindl, Philipp. "Gen-Gen- und Gen-Umwelt-Interaktionsanalysen bei Kindern der multrizentrischen Allergie-Studie." Doctoral thesis, [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=97415766X.

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30

Davey, Edward. "Regulation of cell morphology and adhesion in B lymphocytes by interleukin-4 /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4429-6/.

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31

McKay, Catriona Elizabeth. "Interleukin-4-mediated regulation of CD25 gene expression in human B lymphocytes." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320283.

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32

Mukherjee, Sumanta. "LPS induced TH2 (Interleukin-4) cytokine production in macrophages and its regulation." University of Toledo Health Science Campus / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=mco1207743729.

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33

Yang, Liying. "Targeting Interleukin-4 Receptor α with Hybrid Peptide for Effective Cancer Therapy". Kyoto University, 2014. http://hdl.handle.net/2433/188669.

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Perron, Lepage Marie-France. "Cloning and sequencing of an alternatively spliced variant of bovine interleukin-4 /." [S.l.] : [s.n.], 1999. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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35

Rilka, Jennifer [Verfasser], and Björn [Akademischer Betreuer] Spittau. "Untersuchungen zu altersabhängigen Veränderungen des nigrostriatalen Systems in Interleukin 4-defizienten Mäusen." Freiburg : Universität, 2016. http://d-nb.info/1124004750/34.

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36

Rai, Muhammad Farooq. "Application of IL-4 transgene expression in a chondrocyte based 3D modell of inflammatory arthritis." Berlin Köster, 2008. http://d-nb.info/990051137/04.

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37

Piehler, Daniel [Verfasser], Gottfried [Akademischer Betreuer] Alber, Gottfried [Gutachter] Alber, and Thomas [Gutachter] Göbel. "The inflammatory response against Cryptococcus neoformans is regulated by eosinophilic granulocytes and the interleukin-4/interleukin-4 receptor axis / Daniel Piehler ; Gutachter: Gottfried Alber, Thomas Göbel ; Betreuer: Gottfried Alber." Leipzig : Universitätsbibliothek Leipzig, 2011. http://d-nb.info/1237895855/34.

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38

Pohjanen, V. M. (Vesa-Matti). "Toll-like receptor 4 and interleukin 6 gene polymorphisms in Helicobacter pylori related diseases." Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526212555.

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Abstract Helicobacter pylori is a Gram-negative bacterium, which infects the stomach of more than 50% of the population worldwide. In addition to being the most important risk factor for gastric cancer and peptic ulcers, H. pylori infection is a risk factor for several extra-digestive diseases including dyslipidemia. The consequences of having an H. pylori infection are significantly influenced by the inflammatory response of the host. The pattern recognition receptor Toll-like receptor 4 (TLR4) and the cytokine interleukin 6 (IL6) are important mediators of inflammation in H. pylori related diseases. We have analyzed a series of control subjects and patients with dyspepsia, peptic ulcers or gastric cancer for frequent genetic polymorphisms of the TLR4 and IL6 genes. The prevalence of H. pylori infection, the histologic features of gastritis and cancer and serum endocrine markers and lipid concentrations were also analyzed. Furthermore, the expression of TLR4 was analyzed in specific cell types of gastric mucosa by immunohistochemistry. The TLR4 wild type genotypes of polymorphisms +896 and +1196 were associated with an increased risk of peptic ulcers. The same genotypes also associated with higher serum gastrin levels, but not with atrophy or other features of gastritis. The TLR4 expression was seen in the gastrin and somatostatin secreting cells of gastric mucosa. These results suggest a regulatory link between TLR4 and gastrin secretion. Such a link indicates the presence of a novel effector mechanism for innate immunity in modifying the host endocrine function. The IL6 -174 polymorphism associated significantly with a risk of the diffuse type of gastric carcinoma but not with the intestinal type or its precursor conditions. Finally, we demonstrated that H. pylori infections modify HDL serum levels significantly only in IL6 -174 CC genotype patients, which suggests that the detrimental effects of H. pylori infections on HDL levels are transmitted through IL6. These results clarify the mechanisms of H. pylori related diseases and open new possibilities for research on peptic ulcer disease, gastric cancer and dyslipidemia<br>Tiivistelmä Helicobacter pylori on yleinen ihmisen mahalaukussa esiintyvä Gram-negatiivinen bakteeri. Helikobakteeri on tärkein mahasyövän ja maha- ja pohjukaissuolihaavan riskitekijä ja se on myös muun muassa rasva-aineenvaihdunnan häiriöiden riskitekijä. Ihmisen tulehdusvaste vaikuttaa merkittävästi helikobakteeri-infektion seurauksiin. Tollin kaltainen reseptori 4 (TLR4), joka on hahmontunnistusreseptori ja tulehduksenvälittäjäaine interleukiini 6 (IL6) ovat tärkeitä ihmisen tulehdusvasteeseen osallistuvia proteiineja. Olemme tutkineet dyspepsiaa, maha- ja pohjukaissuolihaavaa ja mahasyöpää sairastavilta potilailta sekä kontrollihenkilöiltä TLR4:n ja IL6:n geenien yleisiä emäsjärjestyksen polymorfioita. Tutkimme myös helikobakteeri-infektion yleisyyttä ja histologisia piirteitä, mahasyövän histologisia piirteitä ja seerumin merkkiaineita ja lipidipitoisuuksia. Lisäksi tutkimme TLR4:n ilmenemistä mahan limakalvolla immunohistokemiallisesti. TLR4:n polymorfismien +896 ja +1196 villin tyypin genotyypit liittyivät kohonneeseen maha- ja pohjukaissuolihaavan riskiin. Samat genotyypit liittyivät myös korkeampiin gastriinitasoihin. TLR4:ä esiintyi mahalaukun limakalvolla gastriinia tai somatostatiinia ilmentävissä soluissa. Täten TLR4:n ja maha- pohjukaissuolihaavariskin yhteys näyttää välittyvän gastriinin erityksen kautta, mikä viittaa uuteen säätely-yhteyteen luontaisen immuniteetin ja mahalaukun umpieritysjärjestelmän välillä. IL6 -174 -polymorfismi yhdistyi diffuusin tyypin mahakarsinooman riskiin mutta ei intestinaalisen tyypin karsinooman riskiin. Helikobakteeri-infektio yhdistyi pienentyneisiin HDL-kolesterolipitoisuuksiin vain potilailla, joilla oli IL6 -174 CC genotyyppi, mikä viittaa helikobakteerin kolesterolitasoille haitallisen vaikutuksen välittyvän IL6:n kautta. Nämä tulokset antavat lisätietoa helikobakteerin aiheuttamien sairauksien mekanismeista ja avaavat uusia tutkimuspolkuja myös mahahaavan, mahasyövän ja rasva-aineenvaihdunnan häiriöiden kliiniseen tutkimukseen
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Levings, Megan K. "Biological and biochemical analyses of the distinctive intracellular signals activated by interleukin-4." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0025/NQ38928.pdf.

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40

Schmidt, Sebastian [Verfasser]. "Einfluss des Interleukin-4-Rezeptors auf den malignen Phänotyp kultivierter Kolonkarzinomzellen / Sebastian Schmidt." Ulm : Universität Ulm, 2019. http://d-nb.info/1200022017/34.

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41

Skog, Emma. "Betydelsen av interleukin 4 receptorn (IL-4R) i stimulering av lymfom- och leukemiceller." Thesis, Malmö högskola, Fakulteten för hälsa och samhälle (HS), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-24758.

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Cytokiner eller interleukiner är signalpeptider med låg molekylär vikt somreglerar många viktiga funktioner. De kan delas in i två grupper beroende på deraseffekt på celler. Interleukin 4 (IL-4) till exempel kan tillhöra gruppentillväxtfaktorer medan interleukin 6 (IL-6) kan tillhöra gruppen aktiverings- ellerdifferentieringsfaktorer. IgM-receptorn eller B-cellsreceptorn, BCR, finns på Bcelleroch är membranbundna immunoglobuliner (mIg) som har tvåhuvuduppgifter; att förmedla signaler som styr B-cellens utveckling samt att bindain antigen som sedan ska presenteras för T-celler. I studien aktiverades B-cellermed antikropp mot IgM (anti-IgM) samt rekombinant IL-4. Efter stimuleringanalyserades IL-6 produktionen med enzyme-linked immunosorbent assay(ELISA). Syftet med studien var att karakterisera uttrycket av IL-4 receptorn pålymfom- och leukemiceller med flödescytometri och polymeras chain reaction(PCR) samt produktion av IL-6 med ELISA. ELISA-analysen visade att tvåcellinjer, stimulerade Sp53 och stimulerade samt kontroller av WaC3CD5+, gaven ökning av IL-6 produktionen. Vid jämförelse med ELISA-resultaten ochflödescytometri-analyserna ser man att WaC3CD5+ som producerat storamängder IL-6, har en liten andel IL-4 receptorer på cellytan. Resultatet av PCRanalysenvisar att det var framförallt Sp53 som fick höga mängder IL-4R mRNA,men även I83, U2932 och WaC3CD5+ fick positiva resultat. Resultaten i dennastudie är preliminära och för att få mer säkerställda resultat krävs att alla analysergörs om ett antal gånger för att få ett mer tillförlitligt resultat.<br>Cytokines or interleukins are signal peptides of low molecular weight, whichregulates many important functions. They can roughly be divided into two groupsor divisions due to their effect on cells. Interleukin 4 (IL-4), for example, belongsto the group growth factors while interleukin-6 (IL-6) belongs to the groupactivation or differentiation factors. IgM receptors or B cell receptors, BCR, areexpressed on B cells and are membrane-bound immunoglobulins (mIg) and havetwo main functions: to convey signals that control B cell activation and to bindantigen which will then be presented to T cells. In the study B cells were activatedwith antibodies against IgM (anti-IgM) and recombinant IL-4. After stimulationthe IL-6 production was analysed by enzyme-linked immunosorbent assay(ELISA). The purpose of this study was to characterize the expression of IL-4receptor in lymphoma and leukemia cells by flow cytometry and polymerasechain reaction (PCR) and furthermore the production of IL-6 by ELISA. ELISAanalysis showed that two cell lines, stimulated Sp53 and stimulated and control ofWaC3CD5+, resulted in an increased IL-6 production. When comparing ELISAresults and flow cytometry assays, it can be seen that WaC3CD5+, whichproduced large amounts of IL-6, has a small percentage of IL-4 receptors on thecell surface. The results of the PCR analysis shows that particularly Sp53displayed high amounts of IL-4 mRNA, but also I83, U2932 and WaC3CD5+were positive for IL-4 mRNA. The results of this study are preliminary, and to getmore trustworthy results, all analyses have to be repeated to get more reliableresults.
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42

Woodward, Eleanor. "Mechanisms by which interleukin-4 suppresses inflammatory cytokine production by activated human monocytes." Thesis, Woodward, Eleanor (2011) Mechanisms by which interleukin-4 suppresses inflammatory cytokine production by activated human monocytes. PhD thesis, Murdoch University, 2011. https://researchrepository.murdoch.edu.au/id/eprint/14844/.

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Improving understanding of how inflammatory responses by monocytes and macrophages are regulated may aid in the development of more targeted therapies for chronic inflammatory disease. In this thesis the mechanisms by which the cytokine, IL-4, can suppress inflammatory cytokine production by LPS-stimulated human monocytes have been examined. IL-4 suppressed LPS-induced TNFα transcription, without inhibiting LPS signalling through IκB, the mitogen-activated protein kinase (MAPK) pathways, or LPS-mediated activation of the transcription factor NF-κB. Histone acetylation regulated LPS-induced cytokine production but not the suppression of these cytokines by IL-4. IL-4 induced three molecules with potential anti-inflammatory properties, suppressor of cytokine signalling-1 (SOCS1), peroxisome proliferator-activated receptor gamma (PPARγ) and triggering receptors expressed on myeloid cells-2 (TREM-2), but suppressed LPS-induced TNFα production independently of these molecules. Targeted gene arrays for Toll-like receptor (TLR) signalling pathways revealed that IL-4 down-regulated mRNA levels of LPS-induced inflammatory cytokines and chemokines, without altering other NF-κB-dependent genes or mRNA levels of TLR-related signalling molecules. Instead, the anti-inflammatory actions of IL-4 may be mediated by up-regulation of an unknown signalling molecule or transcriptional regulator. In LPS-treated monocytes, IL-4 up-regulated mRNA levels for IL-10, receptor-interacting serine-threonine kinase 2 (RIPK2), RP105 and c-Maf. However, the anti-inflammatory actions of IL-4 did not require IL-10 or the kinase activity of RIPK2. While the TLR-homolog, RP105, is likely to negatively regulate LPS responses by monocytes, IL-4 had no effect on cell surface expression of RP105. Additional studies may determine whether c-Maf, a transcription factor which induces IL-10, also regulates the suppression inflammatory cytokine production by IL-4. This study identified novel candidates induced by IL-4 in LPS-stimulated human monocytes. However, the molecules involved in the regulation by IL-4 of LPS-induced TNFα production were not definitively identified. Further studies may identify the mechanisms by which IL-4 is anti-inflammatory. Ultimately, this research will contribute towards the development of novel therapies for inflammatory disease.
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43

MacÃdo, Francisco Yuri BulÃÃo de. "Efeito protetor da interleucina- 4 na cistite hemorrÃgica induzida por ifosfamida em camundongos." Universidade Federal do CearÃ, 2010. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=5159.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior<br>A cistite hemorrÃgica (CH) à um efeito indesejado limitante do uso clÃnico dos agentes quimioterÃpicos do grupo das oxazafosforinas, principalmente ciclofosfamida (CFS) e ifosfamida (IFS). Isto se deve à formaÃÃo de acroleÃna como subproduto do metabolismo dessas drogas. A partir de prÃvios trabalhos conduzidos no LaboratÃrio de Farmacologia da InflamaÃÃo e do CÃncer da Universidade Federal do CearÃ, sabe-se que o Ãxido nÃtrico (NO) atravÃs da ativaÃÃo de iNOS, o fator de ativaÃÃo plaquetÃria, citocinas, como o TNF-&#945; e IL-1&#946;, e prostaglandinas, pela ativaÃÃo da enzima ciclooxigenase-2 (COX-2), sÃo mediadores chave envolvidos nos eventos inflamatÃrios da CH, evidenciados pelo dano urotelial, edema e hemorragia. Sabendo-se que interleucina- 4 (IL- 4) à uma citocina antiinflamatÃria capaz de prevenir a produÃÃo de TNF-&#945;, IL-1&#946; e de atenuar a expressÃo de enzimas inflamatÃrias como iNOS e COX-2, foi investigado se IL- 4 à capaz de reduzir as alteraÃÃes inflamatÃrias vistas na CH induzida por IFS. Para tanto, camundongos Swiss (25-30 g; n=6 por grupo) foram tratados com salina ou IFS (400 mg/kg, ip), e foram analisados por alteraÃÃes no peso Ãmido vesical (PUV), mudanÃas macroscÃpicas e microscÃpicas, alÃm da quantificaÃÃo de edema e hemoglobina vesical. Em outros grupos experimentais, IL- 4 (0,4; 2 ou 10 ng) foi administrada ip uma hora antes à administraÃÃo de IFS. Em outro experimento, camundongos C57BL/6 selvagens e C57BL/6 nocaute para o gene da IL- 4 (-/-) foram tratados com IFS e analisados quanto a mudanÃas no PUV. ImunohistoquÃmica para IL-1&#946; e TNF-&#945;, bem como identificaÃÃo de proteÃnas pela tÃcnica de Western blot para iNOS e COX-2 foram conduzidos nos animais tratados com IL- 4. TambÃm avaliou-se a administraÃÃo de soro anti-IL- 4 (50 Âl/animal, ip) em animais selvagens meia hora antes IFS. Nos animais tratados com IL- 4 (2 e 10 ng), o PUV foi significativamente reduzido em 27% e 39% respectivamente quando comparados ao grupo tratado apenas com IFS. O extravasamento vascular foi reduzido em 29% e 24% e a hemorragia em 47% e 61% nos animais tratados com IL- 4 (2 e 10 ng respectivamente para ambos). A administraÃÃo de IL- 4 exÃgena tambÃm atenuou a expressÃo de TNF-&#945;, IL-1&#946; significativamente, e a expressÃo de iNOS em 27% (dose de 10 ng) e COX-2 em 80% e 76% (doses de 2 e 10 ng, respectivamente), sendo ambos resultados significantes estatisticamente. Em adiÃÃo, animais nocaute para IL- 4 (-/-) e camundongos tratados com soro anti-IL- 4 exibiram um grau de CH pior quando comparados aos camundongos tratados com IFS apenas, em torno de 44% e 28% respectivamente. IL- 4, uma citocina antiinflamatÃria, pode reduzir os fenÃmenos inflamatÃrios vistos na CH induzida por IFS.<br>Hemorrhagic cystitis (HC) is a limiting side effect from the clinic use of chemotherapy agents, mainly cyclophosphamide (CYP) and ifosfamide (IFS). This is due to the fact that acrolein is a urinary metabolite of CYP and IFS, which has been demonstrated to be the causative agent of hemorrhagic cystitis (HC) induced by these compounds. Based on previous experimental studies, most of them from the Laboratory of Pharmacology of Inflammation and Cancer of Federal University of CearÃ, it was demonstrated the participation of inflammatory cytokines such as TNF-&#945;, IL-1&#946;, and the expression of iNOS and COX-2 in ifosfamide-induced HC. Thus, knowing that interleukin-4 (IL- 4) is an anti-inflammatory cytokine able to prevent the production of TNF-&#945;, IL-1&#946;, and decrease the expression of inflammatory enzymes such as iNOS and COX-2, we investigated whether IL- 4 is capable of reducing inflammatory changes seen with ifosfamide-induced HC. For this, male Swiss mice (25-30 g; 6 per group) were treated with saline or ifosfamide (400 mg/kg, intraperitoneally (ip) and analyzed by changes in bladder wet weight (BWW), macroscopic and microscopic parameters, exudate, and hemoglobin quantification. In other groups, IL- 4 (0,4; 2 or 10 ng) was administered ip 1h before ifosfamide administration. In other experimental groups, C57BL/6 WT (wild type) and C57BL/6 WT IL- 4 (-/-) knockout animals were treated with ifosfamide and analyzed for changes in BWW. Immunohistochemistry to TNF-&#945; and IL-1&#946; as well as protein identification by Western blot assay for iNOS and COX-2 were carried out on ifosfamide and IL- 4 treated animals. In other experimental groups, anti-IL- 4 serum was given (50 ÂL/animal, ip) 30 min before ifosfamide. In IL- 4 treated animals, BWW change was significantly less in animals treated with ifosfamide administration only, being reduced by 27% and 39% (2 and 10 ng respectively). Vascular permeability was reduced by 29% and 24%, and hemorrhage by 47% and 61% in those animals treated with IL- 4 (2 and 10 ng respectively). Exogenous IL- 4 also attenuated TNF-&#945;, IL-1 &#946;, iNOS and COX-2 expression on ifosfamide treated bladders. Moreover, knockout animals for IL- 4 (-/-) and animals treated with anti-IL- 4 serum exhibit a more severe degree of inflammation when compared to the wild type mice (approximately 44% and 28% respectively). IL- 4, an anti-inflammatory cytokine, can attenuate the inflammation seen with ifosfamide-induced hemorrhagic cystitis.
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44

Kim, Paul Hyunchul. "Role of 5-Lipoxygenase in Interleukin-4-Induced Oxidative Stress and Inflammation in Vascular Endothelium." Thesis, Virginia Tech, 2010. http://hdl.handle.net/10919/31798.

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Cardiovascular disease (CVD) including atherosclerosis is the leading cause of illness and death in the United States. The American Heart Association indicated that an estimated 81,100,000 American adults have one or more types of CVD and the estimated direct and indirect cost of CVD for 2010 is $503.2 billion, which is $27.9 billion more than last year. Although the exact cause of this disease remains unsolved, previous studies have demonstrated that pro-oxidative and pro-inflammatory pathways in vascular endothelium play a critical role in early pathological events of atherosclerosis. However, the detailed molecular signaling mechanisms underlying this process are not yet completely understood. Recently, the role of interleukin-4 (IL-4) in atherogenesis became controversial and gained attention. IL-4 is a pleiotropic immunomodulatory cytokine secreted by T-helper 2 (Th2) lymphocytes, eosinophils, and mast cells. It was traditionally believed to be an anti-inflammatory cytokine. Increasing evidence, however, has suggested that IL-4 contributes to the initiation and progression of atherosclerosis by oxidative stress-mediated up-regulation of pro-inflammatory mediators such as vascular cell adhesion moledule-1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) in vascular endothelium. 5-Lipoxygenase (5-LOX) is one of the key sources that generate reactive oxygen species (ROS) via metabolic pathways of arachidonic acid. Although 5-LOX has been implicated in the development of atherosclerosis, it remains unclear whether 5-LOX-mediated ROS generation is associated with IL-4-induced MCP-1 expression in vascular endothelium. The present study was focused on the oxidative mechanisms by which IL-4 induces vascular inflammation as well as how 5-LOX is involved in this process. The results showed that IL-4 significantly up-regulates mRNA and protein expression of MCP-1 in vascular endothelium. In addition, DHE and DCF fluorescence staining demonstrated that IL-4 increases ROS production in human vascular endothelial cells. We have also provided the first novel evidence that 5-LOX, one of the enzymes associated with arachidonic acid metabolism, is responsible for the IL-4-induced ROS generation and MCP-1 expression in human vascular endothelial cells.<br>Master of Science
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David, Muriel. "Régulation de l'expression de la chaîne alpha 2 du récepteur de l'IL-13." Paris 6, 2002. http://www.theses.fr/2002PA066089.

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46

Rauch, Kristin Daniela. "Nachweis von Candida – Spezies, Bewertung von Risikofaktoren für eine Vulvovaginalcandidose und Bestimmung der Zytokine Interleukin-1ß, Interleukin-4, Interleukin-6, Interleukin-8 sowie des Leukämie inhibierenden Faktors LIF im Vaginalsekret von schwangeren Frauen mit Verdacht auf eine Vulvovaginalcandidose." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-121998.

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47

Mukherjee, Sumanta. "LPS induced T[subscript]H2 (Interleukin-4) cytokine production in macrophages and its regulation." Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1207743729.

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Dissertation (Ph.D.)--University of Toledo, 2008.<br>"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 161-180.
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Pyle, Angela. "The mechanism of interleukin-4 inhibition of collagen release from cartilage : implications for arthritis." Thesis, University of Newcastle Upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399097.

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49

Brombacher, Tiroyaone M. H. "The role of interleukin-4 receptor alpha on smooth muscle cells during helminth infection." Doctoral thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/12245.

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Includes abstract.<br>Includes bibliographical references (leaves 101-111).<br>Interleukin-4 receptor alpha (IL-4Ra) signaling, mediated by the ligands IL-4 and IL- 13, is important for effective host protection during murine Nippostrongylus brasiliensis (N. brasiliensis) and Schistosoma mansoni (S. manson!) infection. Among other cell types, IL-4Ra responsive smooth muscle cells influence immunological responses and are needed for host protection during N. brasiliensis and S. mansoni infection.
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50

Mohamed, Abdel Rahman Ahmed Nada. "The control of Foxp3+ regulatory T cell by interleukin-4 receptor alpha-mediated signaling." Doctoral thesis, University of Cape Town, 2018. http://hdl.handle.net/11427/29830.

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T regulatory (Treg) cells play a pivotal role in the maintenance of self-tolerance and immune homeostasis. Forkhead box P3 (Foxp3)+ Treg function is controlled by environmental cues of which cytokine-mediated signaling is a dominant component. Recently, Interleukin (IL)-4 has been shown to play an important role in determining the fate of Foxp3+ Tregs. In vivo, IL-4-mediated signaling via Interleukin-4 receptor alpha (IL4Rα) was convincingly shown to mediate Treg transdifferentiation into ex-Foxp3 Th2 or Th17 cells, suggesting a negative regulation of Foxp3+ Tregs by IL-4Rα-mediated signaling. Puzzlingly, however, IL-4-mediated signaling was also independently found to reinforce the Foxp3+ Tregs, counter-arguing for the positive regulation of Foxp3+ Tregs by IL-4Rα-mediated signaling. In the face of such a conundrum, the present work was set forth as an attempt to unambiguously and conclusively decipher the bases of the regulation of Foxp3+ Treg by IL-4Rα-mediated signaling using transgenic murine models. It was first noted that Foxp3+ Treg cells do express IL-4Rα under steady-state. Furthermore, in vitro, purified CD25+ Tregs were prompted to higher Foxp3 expression and increased survival upon stimulation with IL-4 arguing for a potentiating role of IL-4Rα mediated signaling on Foxp3+ Treg cells. To better address the need for the host Foxp3+ Treg cells to express IL-4Rα as observed, we generated Foxp3-specific IL-4Rα deficient mice where IL-4Rα is specifically deleted from Foxp3+ T cells in the whole organism. Even though naïve Foxp3cre IL-4Rα -/lox mice model at homeostasis did neither reveal any significant alteration of the cellular, tissular and phenotypic profile nor development of spontaneous inflammatory disorder when compared to wild-type mice, under S. mansoni infection impairment IL-4Rα-mediated signaling on Foxp3+ Tregs resulted in heightened activation marker expression and elevated T cell effector functions as indicated by increased cytokines production and greater T cell proliferation rate. This heightened immune responsiveness translated overall into an exacerbated parasitic egg-driven fibrogranulomatous inflammation in the liver and the gut of schistosomiasis-diseased Foxp3cre IL-4Rα-/lox mice. Furthermore, in another model of helminth infection with the parasitic nematode, Nippostrongylus brasiliensis, Foxp3cre IL-4Rα-/lox mice showed a higher level of mucus and exaggerated emphysematous pathology in the lungs. Interestingly, the impairment of IL-4Rα signaling within the Foxp3+ Treg population in Foxp3cre IL-4Rα-/lox mice led to a reduced recruitment of Foxp3+ Tregs and a diminished expression of Foxp3, and other associated Treg suppressive markers (i.e. IRF4 and Helios) during the course of these helminth infections. Taken together, our findings supported a role for IL-4Rα signaling in the positive regulation of Foxp3+ Tregs function and thus, the suppression of inflammatory responses during helminth infections. In conclusion, this work demonstrated a positive role for IL-4Rα mediated signaling in the biology of Foxp3+ Treg cells whereby the latter cells require IL-4Rα signaling to survive and maintain Foxp3 expression and suppressive functions so as to efficiently control tissue inflammatory responses during infection. The data presented do provide insights into the mechanisms of Foxp3+ Treg regulation that are highly relevant for the therapeutic control of inflammation during infectious diseases.
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