Дисертації з теми "Tumour necrosis factor receptor I"
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Albataineh, Eman Mohammad. "Studies of tumour necrosis factor receptor-1 in tumour necrosis factor receptor associated periodic sysndrome (TRAPS)." Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537655.
Повний текст джерелаBjörnberg, Flemming. "Processing of TNF-receptors to soluble receptor forms in myeloid cells." Lund : Dept. of Hematology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39176479.html.
Повний текст джерелаVagenas, Panagiotis. "Tumour necrosis factor receptor signalling pathways in chronically activated T lymphocytes." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416631.
Повний текст джерелаWood, Katrina Mackay. "Lymphocyte signalling through members of the Tumour Necrosis Factor Receptor family." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320268.
Повний текст джерелаReddy, Shalini Kamu. "Tumour necrosis factor receptor superfamily memebers in chicken B cell development." Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500214.
Повний текст джерелаKamu, Reddy Shalini. "Tumour necrosis factor receptor superfamily members in chicken B cell development." Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500863.
Повний текст джерелаConnell, Michelle C. "Role of tumour necrosis factor receptor subtypes in endothelial cell inflammatory responses." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430906.
Повний текст джерелаKimberley, Fiona. "A study of the structure and function of tumour necrosis factor receptor superfamily members." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404169.
Повний текст джерелаDrewe, Elizabeth. "Molecular and therapeutic aspects of tumour necrosis factor receptor 1 associated periodic syndrome (TRAPS)." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416437.
Повний текст джерелаTucker, S. J. "Development of novel technologies used to measure tumour necrosis factor receptor signalling in living cells." Thesis, University of Aberdeen, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590943.
Повний текст джерелаPrendergast, D. "Discovery of tumour necrosis factor receptor-1 (p55) binding peptides using a phage display library." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368468.
Повний текст джерелаMohamed, Ahmed A. A. "Cross-talk between kinases and proteases in tumour necrosis factor-#alpha# receptor subtype-induced apoptosis." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274797.
Повний текст джерелаSiebert, Stefan. "Functional characterisation of tumour necrosis factor receptor superfamily 1A (TNFRSF1A) mutations that cause systemic inflammation." Thesis, Cardiff University, 2005. http://orca.cf.ac.uk/55610/.
Повний текст джерелаBertok, Szabolcs. "Tumour necrosis factor-α (TNF) receptor subtype signalling in acute lung injury : a therapeutic approach". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29862.
Повний текст джерелаMcIntosh, Kathryn Ann. "Proteinase-activated receptor-2( PAR-2) and tumour necrosis factor-alpha ( TNFα) signalling in inflammation". Thesis, University of the West of England, Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489251.
Повний текст джерелаJupp, Orla J. "The role of tumour necrosis factor α receptor subtypes in mediating cytosolic phospholipase A2 activation". Thesis, University of Aberdeen, 2000. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602033.
Повний текст джерелаMarles-Wright, Jon. "Structural studies on determinants of receptor/ligand binding in the tumour necrosis factor and T cell receptor protein families." Thesis, University of Oxford, 2005. http://ora.ox.ac.uk/objects/uuid:1f6d480a-a641-4778-9ff0-ece1b2d38d5c.
Повний текст джерелаAbrahams, Vikki Martyne. "The role of immunoglobulin receptors in the pathogenesis of rheumatoid arthritis." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314351.
Повний текст джерелаYouseff, Brian. "The Role of Tumor Necrosis Factor Receptor-Associated Factor 6 in Tick-Borne Flavivirus Infection." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco155691388498993.
Повний текст джерелаColbert, Jeff D. "Compartmentalization of the TNF-Receptor 1-mediated signal transduction /." Connect to full text at ProQuest Digital Dissertations. IP filtered, 2005.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 144-178). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Terry, Jennifer L. "The characterization of TRUSS : a novel scaffolding protein in tumor necrosis factor-[alpha] receptor-1 signaling /." Connect to full text via ProQuest. IP filtered, 2005.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 190-212). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Lobito, Adrian A. "Cell death, stomach pain and migratory rashes : structure-functional analysis of tumour necrosis factor receptor superfamily members in health and disease." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433370.
Повний текст джерелаDuthie, Susan. "Studies of acute phase proteins and tumour necrosis factor receptors as inflammatory markers in the cat." Thesis, University of Glasgow, 1999. http://theses.gla.ac.uk/4809/.
Повний текст джерелаManey, Nicola Jayne. "The regulation of dendritic cell maturation and survival by tumour necrosis factor receptors 1 and 2." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2730.
Повний текст джерелаLubrano, Di Ricco Martina. "The role of tumor necrosis factor receptor family (TNFRF) members in regulatory T cell biology." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS222.
Повний текст джерелаCD4+ Foxp3+ regulatory T cells (Tregs) play a critical role in immune homeostasis and in the prevention of autoimmune diseases by regulating immune responses, therefore a better knowledge of their biology could improve their use in medicine. Different related molecules compose the large TNF family. Many of their receptors (TNFR family) are expressed by cells of the immune system,specifically byTregs.Blocking or agonist reagents of some TNF or TNFR family members have strong potential to control autoimmune diseases or to improve anti-tumor immunity by acting on conventional T cells or Tregs. However, we know very little on the direct effect of TNFR family members on Treg biology and on similarities and differences of their effects between different members. Here, we showed that Treg co-stimulation with agonists of TNFR2, 4-1BB, GITR or DR3, but not of OX40, increased their proliferation and survival. These co-stimulated Tregs had improved expansion in vivo and increased capacity to control an inflammatory disease. Triggering these receptors induced a similar signature at the transcription level, showing that they share signal transduction. Using a DNA binding assay and loss of function approach, we showed a critical role of the canonical NF-B pathway in the Treg co-stimulation induced by these TNFR family members. Thus, these molecules may play a major role in Treg biology and part of the therapeutic effects of drugs targeting TNF or TNFR family members may be Treg-mediated
Mukherjee, Paramita. "Tumor necrosis factor receptor gene therapy influences humoral and cellular immune responses in collagen induced arthritis." Connect to online resource - WSU on-site and authorized users, 2003.
Знайти повний текст джерелаGlossop, John Richard. "Tumour necrosis factor and its receptors in rheumatoid arthritis : relationship between gene polymorphism, cytokine production and disease outcome." Thesis, Keele University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421669.
Повний текст джерелаMoquin, David M. "Elucidating the Molecular Mechanism of CYLD-Mediated Necrosis: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/659.
Повний текст джерелаMoquin, David M. "Elucidating the Molecular Mechanism of CYLD-Mediated Necrosis: A Dissertation." eScholarship@UMMS, 2005. http://escholarship.umassmed.edu/gsbs_diss/659.
Повний текст джерелаZingsheim, Morgan Robert. "Structure-Activity Study of a-N-Methylated SHU9119 Analogues, hMC4R/TNF-a Antagonists, and Mutational Studies of the Melanocyte Stimulating Hormone Receptor." Thesis, The University of Arizona, 2009. http://hdl.handle.net/10150/193426.
Повний текст джерелаGlouchkova, Ludmila. "Biological role of the expression of tumor necrosis factor receptor ligand family molecules on acute leukemia cells." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970363133.
Повний текст джерелаRütten, Simon, Gerald F. Schusser, Getu Abraham та Wieland Schrödl. "Release kinetics of tumor necrosis factor-α and interleukin-1 receptor antagonist in the equine whole blood". Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-205268.
Повний текст джерелаRichter, Fabian [Verfasser], and Roland [Akademischer Betreuer] Kontermann. "Evolution of the antagonistic tumor necrosis factor receptor one-specific antibody ATROSAB / Fabian Richter ; Betreuer: Roland Kontermann." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2015. http://d-nb.info/113823480X/34.
Повний текст джерелаPatel, Brijesh. "The roles of tumour necrosis factor and its receptors in the injury, inflammation and resolution of acute lung injury." Thesis, Imperial College London, 2014. http://hdl.handle.net/10044/1/24695.
Повний текст джерелаSkuland, Trine. "Effects of Toll-like Receptor Agonists and Tumor Necrosis Factor-α in the SW982 Cell Model for Synovitis." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for biologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-21416.
Повний текст джерелаZhou, Wen. "Regulation of Tumor Necrosis Factor-Induced Cell Death and Toll-Like Receptor-Mediated Activation of Macrophages by SPATA2." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17467202.
Повний текст джерелаMedical Sciences
Richter, Christine. "Differential responsiveness of tumour necrosis factor receptors (TNFR) type 1 and 2 : the critical role of the TNFR stalk region." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1284.
Повний текст джерелаRousseau, Adrien. "Tumor necrosis factor Receptor-Associated Factor 4 (TRAF4) est une nouvelle protéine interagissant avec les phosphoinositides, impliquée dans la polarité et la migration cellulaire." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ108/document.
Повний текст джерелаTRAF4 (tumor necrosis factor (TNF) receptor-associated factor 4) is frequently overexpressed in carcinomas suggesting a specific role in cancer. While TRAF4 protein is predominantly found at tight junctions (TJ) in normal mammary epithelial cells (MEC), it accumulates in the cytoplasm of malignant MEC. How TRAF4 is recruited and functions at TJ is unclear. Here we show that TRAF4 possesses a novel phosphoinositide (PIP)- binding domain crucial for its recruitment to TJ. Molecular and structural analyses revealed that the TRAF domain of TRAF4 exists as a trimer which binds up to 3 lipids using basic residues exposed at its surface. Cellular studies indicated that TRAF4 acts a negative regulator of TJ and increases cell migration. These functions are dependent from its ability to interact with PIPs. Our results suggest that TRAF4 overexpression might contribute to breast cancer progression by destabilizing TJ and favoring cell migration
Halford, Emily Elisabeth. "The role of group 3 innate lymphoid cells and tumour necrosis factor receptors in the survival and function of regulatory T cells." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6679/.
Повний текст джерелаRomanatto, Talita. "O Knockout para o receptor 1 de TNF-a protege contra obesidade induzida por dieta." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310352.
Повний текст джерелаTese (doutorado) - Universidade Estadual de Campinas. Faculdade de Ciencias Medicas
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Resumo: O aumento da prevalência de obesidade em várias regiões do planeta é um dos mais importantes fenômenos clínico-epidemiológicos da atualidade. Fatores como a mudança do hábito alimentar e o estilo de vida sedentário, aliados a determinantes genéticos ainda pouco conhecidos desempenham um papel relevante na patogênese dessa doença. Nos últimos quinze anos, desde o descobrimento do hormônio leptina, avanços consideráveis foram obtidos na caracterização dos mecanismos hipotalâmicos do controle da ingestão alimentar e da termogênese. Em um estudo recente demonstrou-se que o consumo de uma dieta rica, em gordura induz a expressão de várias citocinas pró-inflamatórias no hipotálamo e que a inibição da via de sinalização intracelular da serina quinase JNK é capaz de reverter parcialmente algumas das conseqüências clínicas do consumo dessa dieta (De Souza et al, 2005). No presente estudo avaliou-se a importância do receptor 1 de TNF-cc(TNFRI) na gênese do processo inflamatório desencadeado pela dieta rica em gordura. O TNFR1 é responsável pela maioria dos efeitos do TNF-ct, no entanto no contexto da obesidade induzida por dieta, a função desse receptor não está completamente esclarecida. Para tanto, camundongos knockout (KO) para o TNFR1 e seu respectivo background genético, C57BL6, foram tratados por 8 semanas com dieta hiperlipídica e observamos que o TNFR1 KO está protegido da obesidade induzida por dieta por meio de aumento na termogênese. Em ambas as dietas, padrão e hiperlipídica (HF), TNFR1 KO ganha menos peso apesar de aumento na ingestão alimentar. Adiposidade e diâmetro dos adipócitos estão reduzidos, assim como as concentrações sanguíneas de insulina e leptina. TNFR1 KO estão protegidos de resistência hipotalâmica à via da leptina por meio de preservação da sinalização da leptina através de JAK2, STAT3 e FOX01. TNFR1 KO apresentam aumento de termogênese, pelo aumento do consumo de 02, aumento da expressão de UCP-1 e UCP-3, no tecido adiposo marrom e músculo esquelético, respectivamente, e aumento do consumo de O2 de mitocôndrias isoladas de músculo. Isso demonstra que a via de sinalização do TNF-a pelo TNFR1 representa um importante mecanismo envolvido na termogênese deficiente associada à obesidade.
Abstract: In diet-induced obesity, hypothalamic and systemic inflammatory factors trigger intracellular mechanisms that lead to resistance to the main adipostatic hormones, leptin and insulin. Tumor necrosis factor-alpha (TNF-a) is one of the main inflammatory factors produced during this process and its mechanistic role as an inducer of leptin and insulin resistance has been widely investigated. Most of TNF-a inflammatory signals are delivered by TNFR1; however, the role played by this receptor in the context of obesity-associated inflammation is not completely known. Here, we show that TNFR1 knockout (TNFR1 KO) mice are protected from diet-induced obesity due to increased thermogenesis. Under standard rodent chow or ligh-fat diet, TNFR1 KO gain significantly less body mass in spite of increased caloric intake. Visceral adiposity and mean adipocyte diameter are reduced and Dlood concentrations of insulin and leptin are lower. Protection from hypothalamic eptin resistance is evidenced by increased leptin-induced suppression of food ntake and preserved activation of leptin signal transduction through JAK2, STAT3 jnd FOX01. Under high fat diet, TNFR1 KO mice present a significantly increased expression of the thermogenesis-related neurotransmitter, TRH. Further evidence if increased thermogenesis includes the increased 02 consumption and C02 traduction in respirometry measurements, increased expressions of UCP1 and JCP3 in brown adipose tissue and skeletal muscle, respectively, and increased 02 onsumption by isolated skeletal muscle fiber mitochondria. This demonstrates that 'NF-ct signaling through TNFR1 is an important mechanism involved in obesity-ssociated defective thermogenesis.
Doutorado
Medicina Experimental
Doutor em Fisiopatologia Medica
Berkhout, Laura Katharina [Verfasser], and Gisa [Akademischer Betreuer] Tiegs. "Role of Tumor necrosis factor receptor 1 in a mouse model of chronic liver inflammation / Laura Katharina Berkhout ; Betreuer: Gisa Tiegs." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2020. http://d-nb.info/1214370373/34.
Повний текст джерелаMiller, Katherine. "Genetic susceptibility in Alzheimer's Disease and the role of lipid metabolism." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1164830757.
Повний текст джерела[School of Medicine] Department of Epidemiology and Biostatistics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
Heigl, Ulrike [Verfasser], and Wulf [Akademischer Betreuer] Schneider. "Impact of tumor necrosis factor receptor-1 signalling to Listeria monocytogenes-containing phagosomes and its role for bacterial eradication / Ulrike Heigl. Betreuer: Wulf Schneider." Regensburg : Universitätsbibliothek Regensburg, 2011. http://d-nb.info/1030177740/34.
Повний текст джерелаKarathanasis, Christos [Verfasser], Mike [Akademischer Betreuer] Heilemann, Mike [Gutachter] Heilemann, and Gerhard [Gutachter] Hummer. "Quantitative photoactivated localization microscopy reveals the oligomeric state of the tumor necrosis factor receptor 1 / Christos Karathanasis ; Gutachter: Mike Heilemann, Gerhard Hummer ; Betreuer: Mike Heilemann." Frankfurt am Main : Universitätsbibliothek Johann Christian Senckenberg, 2019. http://d-nb.info/1202297951/34.
Повний текст джерелаGaldino, Júnior Hélio. "Produção de fator de necrose tumoral (TNF) em hemoculturas humanas induzida por agonistas de TLR2 (toll-like receptor 2): modulação pelo fator ativador de plaquetas (PAF)." Universidade Federal de Goiás, 2008. http://repositorio.bc.ufg.br/tede/handle/tede/5424.
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Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq
Microorganisms express conserved molecules which ones activate the innate immune system. These molecules are known as pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide (LPS) and bacterial lipoproteins. The PAMPs can be recognized by Toll-like receptors (TLR). The innate immunity activation through TLR pathway induces pro-inflammatory cytokines and lipid mediators, as tumor necrosis factor (TNF) and platelet-activating factor (PAF), respectively. Several reports showed the interaction between TLR4 and PAF receptor (PAFR) signaling to the TNF production; however, the interaction between PAF and other TLR was poorly investigated. The aim of this study was to evaluate the PAF regulatory activity on TLR2-induced TNF production. Thus, Mycoplasma fermentans PG 18 lipoproteins (LAMPf), TLR2/TLR6 agonists and Pam3Cys, a synthetic lipopeptide agonist of TLR2/TLR1 were added to human whole blood cultures and TNF was evaluated by enzyme-linked immunosorbent assay. To evaluate the effects of endogenous PAF on TNF production, a PAF receptor antagonist, WEB2170 was used, and to evaluate the effect of exogenous PAF, PAF was added to the cultures. The blood cultures were also activated with Gram-positive or negative heat-killed bacteria (Staphylococcus aureus or Escherichia coli). The TLR2 expression on polymorphonuclear (PMN) and monocytes were evaluated by flow cytometry, analyzing total cellularity for PMN and CD14+ cells for monocytes. LAMPf, Pam3Cys or LPS induced TNF and the treatment with WEB2170 increased TNF production after TLR2 activation, but not after TLR4 activation. Priming of the blood cultures with PAF up regulated TLR2- induced TNF production. Addition of PAF did not alter TNF release induced by LPS. E. coli induced higher levels of TNF than S. aureus and the treatment with WEB2170 lead to a significant reduction of S. aureus-induced TNF release. However, addition of PAF did not significantly alter bacteria-induced TNF production. With E. coli neither treatment with WEB2170 nor with PAF modulated TNF release. Results indicate that PAF can increase or decrease TNF production induced by TLR2 depending on the time when PAF is combined with TLR2. The increase of the TNF production after extended priming with PAF it was not caused by an increase in TLR2 expression. Thus, it is suggested that interaction between PAFR and TLR2 signaling determines the levels of TNF release. TLR2/PAF/TNF signaling pathway can be relevant in innate immune responses against Gram positive bacteria as well as in inflammatory diseases.
Os microrganismos expressam moléculas conservadas que ativam as células do sistema imune inato. Estas são conhecidas como padrões moleculares associados aos patógenos (PAMPs), tais como o lipopolissacarídeo (LPS) e as lipoproteínas bacterianas. Estes PAMPs são reconhecidos por receptores da família dos Toll-like receptors (TLR). A ativação das células da imunidade natural via TLR induz a produção de citocinas e mediadores lipídicos pro-inflamatórios dentre eles, o fator de necrose tumoral (TNF) e o fator ativador de plaquetas (PAF), respectivamente. A modulação da produção de TNF induzida por agonista de TLR4 (o LPS), pelo PAF, é conhecida, no entanto, a interação entre PAF e outros TLR foi pouco investigada. O presente trabalho teve o objetivo de avaliar a atividade moduladora do PAF na produção de TNF induzida por agonistas de TLR2. Para isto, foram utilizados as lipoproteínas de Mycoplasma fermentans PG 18 (LAMPf), agonistas de TLR2/TLR6 e o Pam3Cys, um lipopeptídeo sintético agonista de TLR2/TLR1. Culturas de sangue total periférico humano foram ativadas com os agonistas de TLR2 ou TLR4 e o TNF foi avaliado nos sobrenadantes, por meio do ELISA. Para avaliar os efeitos do PAF endógeno na produção do TNF, foi utilizado o antagonista do receptor do PAF (PAFR), o WEB2170, e para avaliar o efeito do PAF exógeno, o PAF foi adicionado às hemoculturas. As hemoculturas também foram ativadas com bactérias inteiras (S. aureus ou E. coli) inativadas pelo calor. A expressão de TLR2 em polimorfonucleares (PMN) e monócitos foi avaliada por citometria de fluxo, analisando a celularidade total para os PMN e as células CD14+, para os monócitos. As LAMPf, Pam3Cys ou LPS induziram TNF nas hemoculturas. O tratamento com WEB2170 aumentou a produção de TNF nas hemoculturas estimuladas com agonistas de TLR2, mas não de TLR4. A pré-estimulação das hemoculturas com o PAF aumentou a produção de TNF induzida pelos agonistas de TLR2. A adição de PAF não causou alterações significantes na produção de TNF induzida pelo LPS. Nos ensaios com as bactérias inteiras, E. coli induziu maiores concentrações de TNF do que S. aureus. O tratamento com WEB2170 das hemoculturas estimuladas com S. aureus reduziu a produção de TNF, no entanto, a adição de PAF não alterou significantemente a produção de TNF nas hemoculturas estimuladas com as bactérias. Para E. coli, nem o tratamento com WEB2170, nem com o PAF alterou significantemente a produção de TNF. Os resultados indicam que o PAF pode aumentar ou diminuir a produção de TNF induzida por agonista de TLR2, dependendo do momento em que ele ativa o PAFR em relação à ativação do TLR2. O aumento da produção de TNF após prolongada pré-ativação das hemoculturas com o PAF não foi devido a um aumento na expressão de TLR2. Assim, é sugerido que a interação entre as vias bioquímicas de sinalização do PAFR e do TLR2 determina o nível de produção de TNF. A via de sinalização TLR2/PAF/TNF pode ser importante na imunidade inata contra infecções causadas por bactérias Gram positivas tão bem quanto em doenças inflamatórias.
Dinnetz, Joyce Marie. "Omega-3 fatty acid supplementation reduces basal TNFalpha but not toll-like receptor stimulated TNFalpha in full sized and miniature mares." Thesis, Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/1497.
Повний текст джерелаThangarajh, Mathula. "B-cell-survival factors in multiple sclerosis and myasthenia gravis /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-097-8/.
Повний текст джерелаZhou, Xueyuan. "Follicular Dendritic Cells, Human Immunodeficency Virus Type 1, and Alpha 1 Antitrypsin." BYU ScholarsArchive, 2012. https://scholarsarchive.byu.edu/etd/3407.
Повний текст джерелаBradburn, Jennifer Elizabeth. "Reactive species promotion of head and neck squamous cell carcinoma." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1166555968.
Повний текст джерелаHossain, Akter. "Studies on Redox-proteins and Cytokines in inflammation and Cancer." Doctoral thesis, Linköping : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-8798.
Повний текст джерела