Дисертації з теми "Immunity and Inflammation"
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Wuttge, Dirk Marcus. "Cellular immunity and inflammation in atherosclerosis /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-7349-051-2/.
Повний текст джерелаSalzano, Sonia. "Redox regulation of inflammation and immunity." Thesis, University of Brighton, 2013. https://research.brighton.ac.uk/en/studentTheses/f28a2a37-9169-4b2a-abe8-ee83c6bfe86f.
Повний текст джерелаRagheb, Ramy. "Etude de l'intéraction entre inflammation et infection chez la drosophile." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4104.
Повний текст джерелаWiddrington, John David. "The role of mitochondria in innate immunity and inflammation." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3196.
Повний текст джерелаBlohmke, Christoph Johannes. "Innate immunity and inflammation in cystic fibrosis lung disease." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34559.
Повний текст джерелаMazdai, Goudarz. "The influence of mineral nutrients on immunity and inflammation." Thesis, University of Ulster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281215.
Повний текст джерелаCroft, Nicholas Michael. "Investigation of gastrointestinal mucosal immunity and inflammation in children." Thesis, University of Edinburgh, 1996. http://hdl.handle.net/1842/21172.
Повний текст джерелаPhan, Quang Tien. "Innate immune response to tissue-specific infection : notochord infection in the zebrafish embryo." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT082/document.
Повний текст джерелаIn bacterial infections, according to the infected tissue and the nature of pathogens, the body responds by mobilizing various actors. I decided to use zebrafish or Danio rerio model to study the innate immune response to bacterial infection in the situations that professional phagocytes cannot come in direct contact with the bacteria. For this, I developed a model of infection in the notochord of zebrafish embryo. Upon injection of bacteria in this compartment, the microbes find themselves protected by the thick collagensheath where the phagocytes cannot penetrate. While mycobacteria are not detected by phagocytes; E. coli bacteria are sensed and a significant local inflammation around the notochord is mounted. The E. coli, although inaccessible to phagocytosis are eliminated within the first 24 hours after injection, the inflammation lasts several days.I studied the mechanisms that lead to this persistent inflammation and its long term consequences on the development of the fish. I showed the central role of the cytokine IL1B in this process, and I developed a transgenic line that allows studying in vivo the induction of this cytokine in fish.I then studied the roles of the two main populations of phagocytes in the elimination of E. coli. I revealed that macrophages are not involved in the removal of bacteria but neutrophils, although unable to penetrate inside the collagen casing, are necessary for the bacterial elimination. I also confirmed that myeloperoxidase and nitrogen monoxide are not involved in the removal of bacteria, rather the reactive oxygen species produced by neutrophils are needed to eradicate the infection
Ellouze, Mehdi. "Identification des mécanismes anti-inflammatoires de GILZ dans les monocytes/macrophages et de son potentiel thérapeutique dans le choc septique." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS239/document.
Повний текст джерелаSepsis and septic shock, associated with a severe and uncontrolled systemic inflammation, are the main causes of death in intensive care units. Macrophages play a central role in these pathologies. They are involved in the initiation and regulation of inflammation. They recognize LPS from the bacterial cell wall via TLR4, which triggers the activation of MAPK signaling pathway and transcription factors such as NF-KB and AP1 and ultimately, the production of pro-inflammatory cytokines including TNF and IL6. The expression of the protein GILZ in macrophages limits in vitro the production of IL6 and TNF in response to LPS. This effect is attributed to inactivation of NF-kB. Moreover, GILZ expression decreases in human and mouse macrophages exposed to LPS.Given the regulatory effects of GILZ in macrophages, the objectives of our study were 1) to determine whether GILZ expression is down-regulated in monocytes / macrophages (M/M) in the sepsis, 2) to determine whether the modulation of GILZ expression in M/M is sufficient to influence systemic inflammation, and 3) to identify GILZ mechanism of action in human M/M.GILZ expression was measured in the M/M of patients with septic shock or acute respiratory distress syndrome, and in a murine model of endotoxemia. We observed a significant reduced expression of GILZ in these pathological contexts in human and mice. The impact of this alteration was explored in unique transgenic mouse model in which macrophages stably overexpress GILZ (CD68-GILZ).We confirmed that GILZ overexpression limits TNF production and promotes IL-10 production in in vitro LPS-stimulated macrophages. We further studied the inflammatory response and survival of these mice in models of endotoxemia and septic shock. We showed that GILZ overexpression restricted to macrophages, limits serum pro-inflammatory cytokines production, therefore decreases systemic inflammation and significantly improves mice survival. These results highlight the effects of macrophage polarization by GILZ at a systemic level.This result confirmed the need to characterize GILZ interactome in human macrophages. Two complementary approaches have been used. The first one consists of a pan-genomic double hybrid screening of human GILZ partners. The second method consists of a tandem affinity purification (TAP-TAG) of GILZ protein and its associated partners, followed by the identification of these partners by mass spectrometry. Analyses have been performed independently on nuclear and cytoplasmic extracts from human macrophage cells, genetically engineered to express GILZ protein with the two tags required for purification. This dual approach led us to identify new direct and indirect interactions between GILZ and other key proteins of TLR4 signaling pathway in human macrophages and highlight a likely role of GILZ as a transcription regulatory factor.These results confirm the anti-inflammatory role of GILZ on systemic inflammation and enhancement of lifetime in murine models of endotoxemia and septic shock. Furthermore, this work identifies for the first time the cytoplasmic and nuclear GILZ partners in human macrophages and would allow in the future, a better understanding of GILZ mechanism of action
Lajunen, T. (Taina). "Persistent Chlamydia pneumoniae infection, inflammation and innate immunity." Doctoral thesis, University of Oulu, 2008. http://urn.fi/urn:isbn:9789514289965.
Повний текст джерелаCampos-Pereira-Da-Cruz-Viana, Joao. "Exercise in chronic kidney disease : impact on immunity and inflammation." Thesis, Loughborough University, 2011. https://dspace.lboro.ac.uk/2134/9090.
Повний текст джерелаThursfield, Rebecca Marie. "Infection, inflammation & innate immunity in the paediatric CF airway." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/43757.
Повний текст джерелаChan, Calvin. "Uncovering an Adipocyte’s Perspective of Inflammation and Immunity in Obesity." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1560866472579872.
Повний текст джерелаSermersheim, Matthew Alan. "MG53 is a Novel Regulator of Inflammation and Innate Immunity." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu157121945938419.
Повний текст джерелаSrinivasan, N. "The role of inflammasomes in intestinal inflammation." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:04ad577c-a8dd-46eb-811a-79a3980ff806.
Повний текст джерелаLensmar, Catarina. "Early airway inflammation in allergic asthma : aspects of pulmonary innate immunity /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4463-6/.
Повний текст джерелаBordon, Yvonne. "The role of the D6 chemokine receptor in immunity and inflammation." Thesis, University of Glasgow, 2007. http://theses.gla.ac.uk/6552/.
Повний текст джерелаBlackshaw, Sasha. "The manipulation of inflammation, immunity and infection by novel derivatives of halichlorine." Thesis, Manchester Metropolitan University, 2017. http://e-space.mmu.ac.uk/618825/.
Повний текст джерелаYuan, Ruoxi. "Dynamic Programming of Innate Immunity in Health and Disease." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/82925.
Повний текст джерелаPh. D.
Philipson, Casandra Washington. "Systems analysis and characterization of mucosal immunity." Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/74392.
Повний текст джерелаPh. D.
Roberts, Morgan. "The role of the Lyn tyrosine kinase in innate immunity and intestinal inflammation." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54079.
Повний текст джерелаScience, Faculty of
Microbiology and Immunology, Department of
Graduate
Iracheta-Vellve, Arvin. "Innate Immunity As Mediator of Cell Death and Inflammation in Alcoholic Liver Disease." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/960.
Повний текст джерелаLiu, Yi-Hsia. "Novel functions of Tribbles 1 in macrophages." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/8159.
Повний текст джерелаChan, James. "Upregulation of early inflammation to enhance fracture repair." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:19ccec9a-ea37-4ece-b083-0f339d7178ed.
Повний текст джерелаAmbrose, Timothy James William. "Serine hydrolase activity and roles for monoacylglycerol lipase in innate immunity and intestinal inflammation." Thesis, University of Oxford, 2018. http://ora.ox.ac.uk/objects/uuid:f7a12796-ae8f-4121-ab1a-26778261ac78.
Повний текст джерелаKlarquist, Jared. "Type I IFN control of sterile inflammation: Uncovering mechanisms behind autoimmunity and antitumor immunity." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1467988023.
Повний текст джерелаKowalski, Elizabeth Ashley. "Toll-Interacting Protein Regulation of Low-grade Non-resolving Inflammation." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/78340.
Повний текст джерелаPh. D.
Zhao, Junjie. "MECHANISMS OF SINGLE IG IL-1-RELATED RECEPTOR MEDIATED SUPPRESSION OF COLON TUMORIGENESIS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1459761067.
Повний текст джерелаMaurer, Kirk J. "A systematic evaluation of the role of infection, immunity and inflammation in cholesterol gallstone pathogenesis." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/39917.
Повний текст джерелаIncludes bibliographical references.
Cholesterol gallstones are exceptionally common and cost nearly 10 billion U.S. dollars annually. Despite a half-century of basic and clinical research questions still remain about cholesterol gallstone pathogenesis. The purpose of the study presented herein is to analyze the roles of infection, and immunity in cholelithogenesis. The first two aims of this work were to analyze the role of enterohepatic Helicobacter spp. and the human gastric pathogen H. pylori in cholesterol gallstone formation. To test this, we prospectively infected C57UJ mice with a variety of Helicobacter spp. and fed infected and uninfected mice a lithogenic diet for eight weeks and analyzed biliary phenotype. Mice infected with H. bilis or coinfected with H. hepaticus and H. rodentium and fed a lithogenic diet developed cholesterol gallstones at 80% prevalence compared with approximately 10% in uninfected controls (P<0.05). Monoinfections with H. hepaticus, H. cinaedi, H. rodentium, and H. pylori gave a cholesterol gallstone prevalence of 40% (P<0.05), 30%, 20% and 20%, respectively; with the exception of H. hepaticus, cholesterol gallstone formation in these groups did not differ significantly from uninfected animals.
(cont.) These findings suggest that some Helicobacter spp. play a role in the cholesterol gallstone formation in mice and perhaps humans. We further hypothesized that inflammation and immunity were important in cholesterol gallstone formation and that cholelithogenic bacteria were promoting gallstones through immune stimulation. To test this we utilized BALB/c and isogenic Rag2-/- mice. When fed a lithogenic diet for eight-weeks, wild-type mice developed cholesterol gallstones (27-80% prevalence) significantly more than Rag2-/- mice (~5%, P<0.05). Transfer of functional splenocytes, or T-lymphocytes to Rag2-/- mice markedly increased cholesterol gallstone formation (26% and 40% respectively, P<0.05) whereas transfer of B-cells did not (13%). The presence of T-cells and solid cholesterol monohydrate crystals induced proinflammatory cytokine expression in the gallbladder. These studies indicate that T-cells are critical in murine cholelithogenesis and function by promoting gallbladder inflammation. In summary, these results illustrate that microbial pathogens can influence cholesterol gallstone formation; this most likely occurs by modulating the immune response with T-cells being a critical component in this immunomodulation.
by Kirk J. Maurer.
Ph.D.
Berlanga-Taylor, Antonio Jorge. "Impact of genetic variation on gene regulatory effects of vitamin D in immunity and inflammation." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:0f4679e7-7ef6-49e6-ab04-5fc280f1d680.
Повний текст джерелаJangalwe, Sonal. "Regulation of Alloreactive CD8 T Cell Responses by Costimulation and Inflammation." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/907.
Повний текст джерелаPatel, Rajen. "Dendritic Cells Mediate Protective Immunity Against Salmonella Typhimurium by Regulating Antigen Presentation, Inflammation and Cell Death." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34307.
Повний текст джерелаYuan, Kai. "Metabolic inflammation and immunomodulation in dairy cows." Diss., Kansas State University, 2014. http://hdl.handle.net/2097/17294.
Повний текст джерелаDepartment of Animal Sciences and Industry
Barry J. Bradford
The transition period in dairy cows is characterized by dramatic increases in nutrient requirements for lactation and substantial metabolic stress. The disturbed metabolic balance, coupled with suppressed immune function, contributes to markedly elevated incidence of health disorders. Several lines of evidence suggest that increased inflammation is common during the transition period. Unlike the classical inflammation associated with acute infection, the postpartum inflammatory state is low-grade and often of metabolic origin. This metabolic inflammation plays a key role in numerous disorders; an improved understanding of inflammatory pathways in transition cows may improve our ability to predict and prevent disorders. To mimic metabolic inflammation, in Experiment 1, we administered low amounts of recombinant bovine tumor necrosis factor-α (rbTNFα), a pro-inflammatory cytokine, to early lactation cows, and evaluated whether rbTNFα affects milk production, metabolism, and health. We found that rbTNFα administration increased systemic inflammation, decreased feed intake and milk yield, and increased incidence of disorders. Conversely, preventing excessive inflammation has the potential to improve productivity and health of dairy cows. To identify nutritional strategies that could enhance metabolism and immunity, we evaluated the efficacy of several feed additives. In Experiment 2, we evaluated effects of chromium propionate, rumen-protected lysine and methionine, or both on metabolism and immunity in lactating dairy cows, and found that supplementation of these nutrients may enhance neutrophil function. In Experiment 3, we determined whether supplementation of yeast product to transition cows could enhance production, metabolism, and immunity, and found that yeast product modulated feeding behavior, metabolism, immunity, and uterine inflammation. Overall, a greater understanding of the role of metabolic inflammation in the transition period and the nutritional strategies that could modulate these signals may improve the production and health of dairy cows.
Wachholz, Kristina Lora Catherine. "Placental Infection by Salmonella Typhimurium in a Murine Model: The Role of Innate Immune Mediators in Cell Death at the Fetal-Maternal Interface." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34190.
Повний текст джерелаWu, Salene M. "Relationship of General and Health-related Anxiety and Worry to Markers of Inflammation in Women with Advanced Cancer." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1356624916.
Повний текст джерелаWiggins, Kimberley Anne. "Novel proteases that regulate interleukin-1 alpha activity during inflammation and senescence." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/273664.
Повний текст джерелаJanczy, John Roger. "Mechanisms for activation and inhibition of inflammasomes." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1643.
Повний текст джерелаGicquel, Thomas. "Implication des récepteurs purinergiques dans l'activation de l'inflammasome NLRP3 dans les macrophages." Thesis, Rennes 1, 2014. http://www.theses.fr/2014REN1B012/document.
Повний текст джерелаNLRP3-inflammasome pathway activation appears as the corner stone of manyinflammatory diseases including pulmonary fibrosis, rheumatoid arthritis, gout and Crohn disease. This pathway is known to be activated by danger signals such as ATP or Monosodium urate (MSU) leading to the pro-inflammatory cytokine IL-1β release. The aim of this study is to investigate the role of purinergic receptors in the activation of NLRP3-inflammasome pathway in human macrophages. We found here that MSU or analogs of ATP (ATPγS or BzATP) induced the release of IL-1β from LPS-primed MDM obtained from buffy coat (EFS, Rennes). We observed that purinergic P2X7 receptor antagonists, cathepsin B or caspase-1 inhibitors, siRNA targeting P2Y2R or P2X7R were able to reduce the release of IL-1β from activated macrophages. Furthermore we studied the role of purinergic receptors in pro-inflammatory cytokines release, such as IL-1α or IL-6. This study suggests that P2 receptors-NLRP3 inflammasome pathway represents a novel potential therapeutic target to control inflammation in inflammatory diseases
Lemaitre, Julien. "Heterogeneity of polymorphonuclear neutrophils in HIV-1 infection. Study of SIV-infected cynomolgus macaque model." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS267.
Повний текст джерелаEven under combinational antiretroviral treatments (cART), HIV-1 persistence is associated with chronic inflammation in infected patients, leading to an increased risk of non-AIDS-related comorbidities. Polymorphonuclear neutrophils (PMN), have been less studied in HIV infection whereas they were associated with chronic inflammation diseases. To evaluate PMN heterogeneity in SIVmac251 nonhuman primate infection model, we first performed multiparameter single-cell phenotyping by mass cytometry giving a global vision of the immune system. This analysis demonstrated circulation of immature PMN with impaired during chronic infection. Then, we characterized neutrophils heterogeneity in the course of SIV infection. In primary infection, there was an increased frequency of CD10- immature and CD62L-low primed PMNs in peripheral blood. In chronic phase, CD10- immature PMNs were significantly higher in bone marrow and blood, maintaining a primed profile. During SIV infection, PMNs demonstrated variable immunomodulatory function against T cells proliferation and cytokine production. Early cART allowed to restore PMN phenotype. In this study, we provide unprecedented insight into PMN heterogeneity in the course of SIV infection. Since PMN represent 40-70% of circulating leukocytes and primed PMN are more potent to release pro-inflammatory cytokines and to transmigrate, they should be considered as a new player in HIV-1 chronic inflammation
Cammarata-Mouchtouris, Alexandre. "Régulation des voies NF-KB au cours de la réponse immunitaire innée." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ118.
Повний текст джерелаThe innate immune system is a defense mechanism common to all metazoans. lts activation can be deleterious when it is uncontrolled. The study of the mechanisms underlying this balance between the activation or not of the innate immune response is the basis of my thesis work. The similarity of the molecular pathways - such as the NF-KB pathway - relaying the innate immune response in insects and mammals makes Drosophila an excellent model for exploring the immune response.After immune stimulation, stopping the molecular pathways of immunity is necessary to prevent the development of autoimmune diseases or cancer. My first project focused on understanding a time-dependent mode of regulation in one of Drosophila's NF-KB pathways. My second project concerns the activation of the immune response. A nuclear protein contrai the involvement of epigenetic machinery in controlling the expression of one of Drosophila's NF-KB pathways. Ali this makes it possible to better grasp the dynamics of regulation of the innate response
Lansink, Lianne Ida Maria. "Blood-stage Plasmodium parasite control by antibody-mediated inhibition and impaired maturation in response to host inflammation in vivo." Thesis, Queensland University of Technology, 2022. https://eprints.qut.edu.au/228523/1/Lianne%20Ida%20Maria_Lansink_Thesis.pdf.
Повний текст джерелаSävykoski, née Huittinen T. (Tiina). "Chlamydia pneumoniae infection, inflammation and heat shock protein 60 immunity in asthma and coronary heart disease." Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514269853.
Повний текст джерелаBonnay, François. "Caractérisation des mécanismes de régulation de la voie IMD au cours de la réponse immunitaire chez Drosophila melanogaster." Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ019/document.
Повний текст джерелаThe innate immune response is required by all metazoan to defend themselves against microorganisms. When abnormally activated however, innate immune responses cause deleterious chronic inflammation. The study of the fragile equilibrium between immune responses and tolerance has fundamentally shaped the projects of my PhD work.First, using Drosophila melangoaster as a model, I characterized Big-Bang as a major player of the immune balance in the gut. I could show that Big-Bang is a bona fide component of midgut epithelium septate junctions. Consequently, big-Bang deficient flies have an impaired tolerance against commensal microorganisms and are susceptible to invasive gut pathogens, ultimately leading to a premature death of flies.I focused the second part of my PhD work on the characterization of Akirin, a nuclear protein required for the activation of NF-ΚB response from Drosophila to humans. My results showed that Akirin is a selector molecule, acting together with NF-ΚB and the SWI/SNF chromatin-Remodeling complex to sustain the transcription of a subset of pro-Inflammatory genes
Patrick, Christopher. "Cereal Induced Autoimmune Diabetes is Associated with Small Intestinal Inflammation, Downregulated Anti-Inflammatory Innate Immunity and Impaired Pancreatic Homeostasis." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/30391.
Повний текст джерелаFang, Youjia. "The Novel Role of Interleukin-1 Receptor-Associated Kinase 1 in the Signaling Process Controlling Innate Immunity and Inflammation." Thesis, Virginia Tech, 2009. http://hdl.handle.net/10919/32331.
Повний текст джерелаMaster of Science
Liu, Chia-Fang. "The role of surfactant protein D in the Der p allergen-induced inflammation in the innate immunity of lung." Toulouse 3, 2008. http://thesesups.ups-tlse.fr/580/.
Повний текст джерелаAllergic asthma is a disease of chronic airway inflammation. Dermatophagoides pteronyssinus (Der p) is among the most prominent and important allergens that cause allergic asthma around the world. However, the mechanism of Der p-induced inflammation in the innate immunity of lung is not fully understood. Surfactant protein D (SP-D) plays an important role in the first-line defense of the lung. In summary, we found that (1) SP-D had a therapeutic effect on allergen-induced bronchial inflammation in the murine model of asthma. (2) Mite allergen-induced alveolar macrophage activation was mediated by CD14 /TLR4 and TLR2 and could be inhibited by SP-D pretreatment. (3) Der p allergen induced NF-?B-dependent pro-inflammatory mediators production, and prevented endotoxin-induced IL-12 and T-bet production through TLR2/4 co-activation in mouse alveolar macrophage cell line, and (4) SP-D inhibited Der p-induced inflammatory signaling pathway and inflammatory mediators production through regulating DC-SIGN expression in acting as an inhibitory signal to inhibit Der p-induced inflammatory response. In conclusion, SP-D, as an important molecule of innate immunity of lung, can regulate allergen-induced pulmonary inflammation. .
Listopad, Joanna Jadwiga. "HO-1 induction by Co-PPIX suppresses experimental skin inflammation, T cell immunity and dendritic cell maturation and function." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15601.
Повний текст джерелаHeme oxygenase 1 (HO-1) is an antiinflammatory stress protein. Its immunosuppressive and cytoprotective activities have been demonstrated in several animal models. The underlying mechanisms, however, are poorly understood. This study demonstrates for the first time that the physiological induction of HO-1 is important for the limitation and resolution of T cell-dependent skin inflammation. So, the HO-1 inhibitor, tin protoporphyrin IX (Sn-PPIX), augments cutaneous inflammation in mouse model. Moreover, pharmacologic HO-1 induction by the potent HO-1 inducer, cobaltic protoporphyrin IX (Co-PPIX), inhibits inflammation when applied around sensitization or before challenge in murine DNFB- and TMA-induced contact hypersensitivity models. Remarkably, Co-PPIX treatment inhibits antigen-driven T cell proliferation both ex vivo in murine splenocytes and in vitro in human peripheral blood mononuclear cells. Since induction of HO-1 mRNA and protein was found in monocytes and monocyte-derived myeloid dendritic cells (MDDC) but not T cells, further investigations focused on antigen-presenting cells. HO-1 induction by Co-PPIX depresses monocytic MHC class II and accessory molecule expression whereas phagocytosis and respiratory burst activities are augmented. Moreover, HO-1 induction inhibits the immunophenotypic differentiation and maturation of MDDC. Functional analysis revealed a decreased proinflammatory cytokine production whereas secretion of the antiinflammatory cytokine IL-10 is increased. Remarkably, the antigen-presenting capacity of MDDC for T-helper cells is diminished both for allo- and for recall-antigens. Adenoviral HO-1 transduction of MDDC confirmed that the effects are mediated by HO-1. These data indicate that an enhanced HO-1 activity switches myeloid DCs to an immature and functionally compromised phenotype and suggest that HO-1 induction represents an important approach for depressing T cell immunity and for the treatment of T cell-dependent skin inflammation.
Baigrie, Robert John. "Cytokine and other components of the integrated host response to injury." Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/26464.
Повний текст джерелаLong, Matthew Eugene. "Manipulation of the innate immune response and evasion of macrophage host defense mechanisms by Francisella tularensis." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1683.
Повний текст джерелаHarbort, Christopher. "Regulation of innate immunity by DNA damage signaling." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2017. http://dx.doi.org/10.18452/17791.
Повний текст джерелаNeutrophils are cells of the mammalian innate immune system whose inflammatory functions are essential for microbial clearance but cause collateral tissue damage. Inflammation is regulated by both pro- and anti-inflammatory signals, including cytokine production and initiation of apoptosis. A cornerstone of the regulation of these functions is the oxidative burst, by which neutrophils generate reactive oxygen species (ROS). The downstream targets of ROS responsible for regulating these functions are not fully identified. We have identified ataxia telangiectasia mutated (ATM) kinase, a master regulator of the DNA damage response (DDR), as a ROS-dependent modulator of neutrophil responses. Mutations in ATM cause the disease Ataxia-telangiectasia (AT). In addition to disorders resulting from defective DNA repair, AT patients suffer from symptoms linked to inflammation, leading us to examine their neutrophil responses. We report that neutrophils from AT patients overproduce pro-inflammatory cytokines and delay apoptosis. We further show that DNA damage in neutrophils suppresses cytokine production and can initiate apoptosis via a mechanism involving ATM, p38, and Chk2. Furthermore, the oxidative burst was required for activation of ATM to regulate these processes.. This work reveals a novel mechanism for the regulation of neutrophil functions, establishing the DDR as a mediator of immune regulation by ROS. Furthermore, it indicates that neutrophil dysregulation may underlie chronic inflammation in AT patients. We propose that inflammation may be a driving force behind some of the pathology of AT, providing a potential target for clinical intervention for some symptoms of this currently untreatable disease.