Relevant bibliographies by topics / Inflammasones

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Inflammasones'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Inflammasones"

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Inoue, Makoto, and Mari L. Shinohara. "NLRP3 Inflammasome and MS/EAE." Autoimmune Diseases 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/859145.

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Inflammasomes are cytosolic sensors that detect pathogens and danger signals in the innate immune system. The NLRP3 inflammasome is currently the most fully characterized inflammasome and is known to detect a wide array of microbes and endogenous damage-associated molecules. Possible involvement of the NLRP3 inflammasome (or inflammasomes) in the development of multiple sclerosis (MS) was suggested in a number of studies. Recent studies showed that the NLRP3 inflammasome exacerbates experimental autoimmune encephalomyelitis (EAE), an animal model of MS, although EAE can also develop without the NLRP3 inflammasome. In this paper, we discuss the NLRP3 inflammasome in MS and EAE development.
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Wagatsuma, Kohei, and Hiroshi Nakase. "Contradictory Effects of NLRP3 Inflammasome Regulatory Mechanisms in Colitis." International Journal of Molecular Sciences 21, no. 21 (October 30, 2020): 8145. http://dx.doi.org/10.3390/ijms21218145.

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The inflammasome is an intracellular molecular complex, which is mainly involved in innate immunity. Inflammasomes are formed in response to danger signals, associated with infection and injury, and mainly regulate the secretion of interleukin-1β and interleukin-18. Inflammasome dysregulation is known to be associated with various diseases and conditions, and its regulatory mechanisms have become of great interest in recent years. In the colon, inflammasomes have been reported to be associated with autophagy and the microbiota, and their dysregulation contributes to colitis and. However, the detailed role of inflammasomes in inflammatory bowel disease is still under debate because the mechanisms that regulate the inflammasome are complex and the inflammasome components and cytokines show seemingly contradictory multiple effects. Herein, we comprehensively review the literature on inflammasome functioning in the colon and describe the complex interactions of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome components with inflammatory cytokines, autophagy, and the microbiota in experimental colitis models and patients with inflammatory bowel disease.
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Spalinger, Marianne R., Marlene Schwarzfischer, and Michael Scharl. "The Role of Protein Tyrosine Phosphatases in Inflammasome Activation." International Journal of Molecular Sciences 21, no. 15 (July 31, 2020): 5481. http://dx.doi.org/10.3390/ijms21155481.

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Inflammasomes are multi-protein complexes that mediate the activation and secretion of the inflammatory cytokines IL-1β and IL-18. More than half a decade ago, it has been shown that the inflammasome adaptor molecule, ASC requires tyrosine phosphorylation to allow effective inflammasome assembly and sustained IL-1β/IL-18 release. This finding provided evidence that the tyrosine phosphorylation status of inflammasome components affects inflammasome assembly and that inflammasomes are subjected to regulation via kinases and phosphatases. In the subsequent years, it was reported that activation of the inflammasome receptor molecule, NLRP3, is modulated via tyrosine phosphorylation as well, and that NLRP3 de-phosphorylation at specific tyrosine residues was required for inflammasome assembly and sustained IL-1β/IL-18 release. These findings demonstrated the importance of tyrosine phosphorylation as a key modulator of inflammasome activity. Following these initial reports, additional work elucidated that the activity of several inflammasome components is dictated via their phosphorylation status. Particularly, the action of specific tyrosine kinases and phosphatases are of critical importance for the regulation of inflammasome assembly and activity. By summarizing the currently available literature on the interaction of tyrosine phosphatases with inflammasome components we here provide an overview how tyrosine phosphatases affect the activation status of inflammasomes.
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Forn-Cuní, Gabriel, Annemarie H. Meijer, and Monica Varela. "Zebrafish in Inflammasome Research." Cells 8, no. 8 (August 15, 2019): 901. http://dx.doi.org/10.3390/cells8080901.

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Inflammasomes are cytosolic multiprotein complexes that regulate inflammatory responses to danger stimuli and infection, and their dysregulation is associated with an increasing number of autoinflammatory diseases. In recent years, zebrafish models of human pathologies to study inflammasome function in vivo have started to emerge. Here, we discuss inflammasome research in zebrafish in light of current knowledge about mammalian inflammasomes. We summarize the evolutionary conservation of inflammasome components between zebrafish and mammals, highlighting the similarities and possible divergence in functions of these components. We present new insights into the evolution of the caspase-1 family in the teleost lineage, and how its evolutionary origin may help contextualize its functions. We also review existing infectious and non-infectious models in zebrafish in which inflammasomes have been directly implicated. Finally, we discuss the advantages of zebrafish larvae for intravital imaging of inflammasome activation and summarize available tools that will help to advance inflammasome research.
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Yi, Young-Su. "Caspase-11 Non-Canonical Inflammasome: Emerging Activator and Regulator of Infection-Mediated Inflammatory Responses." International Journal of Molecular Sciences 21, no. 8 (April 15, 2020): 2736. http://dx.doi.org/10.3390/ijms21082736.

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Inflammation is a body’s protective mechanism to eliminate invading pathogens and cellular damaging signals. The inflammatory response consists of two main consecutive steps—a priming step preparing the inflammatory responses and a triggering step boosting the inflammatory responses. The main feature of the triggering step is the activation of the inflammasome, an intracellular multiprotein complex facilitating the inflammatory responses. The regulatory roles of ‘canonical’ inflammasomes in the inflammatory responses and diseases have been largely investigated, so far. New types of inflammasomes have been recently discovered and named as ‘non-canonical’ inflammasomes since their roles to induce inflammatory responses are similar to those of canonical inflammasomes, however, the stimulating ligands and the underlying mechanisms are different. Therefore, a growing number of studies have actively investigated the novel roles of non-canonical inflammasomes in inflammatory responses and diseases. This review summarizes and discusses the recent studies exploring the regulatory roles of caspase-11 non-canonical inflammasome during the inflammatory responses and provides insight into the development of novel therapeutics for infectious and inflammatory diseases by targeting caspase-11 non-canonical inflammasome.
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Looi, Chin King, Ling-Wei Hii, Felicia Fei-Lei Chung, Chun-Wai Mai, Wei-Meng Lim, and Chee-Onn Leong. "Roles of Inflammasomes in Epstein–Barr Virus-Associated Nasopharyngeal Cancer." Cancers 13, no. 8 (April 8, 2021): 1786. http://dx.doi.org/10.3390/cancers13081786.

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Epstein–Barr virus (EBV) infection is recognised as one of the causative agents in most nasopharyngeal carcinoma (NPC) cases. Expression of EBV viral antigens can induce host’s antiviral immune response by activating the inflammasomes to produce pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and IL-18. These cytokines are known to be detrimental to a wide range of virus-infected cells, in which they can activate an inflammatory cell death program, called pyroptosis. However, aberrant inflammasome activation and production of its downstream cytokines lead to chronic inflammation that may contribute to various diseases, including NPC. In this review, we summarise the roles of inflammasomes during viral infection, how EBV evades inflammasome-mediated immune response, and progress into tumourigenesis. The contrasting roles of inflammasomes in cancer, as well as the current therapeutic approaches used in targeting inflammasomes, are also discussed in this review. While the inflammasomes appear to have dual roles in carcinogenesis, there are still many questions that remain unanswered. In particular, the exact molecular mechanism responsible for the regulation of the inflammasomes during carcinogenesis of EBV-associated NPC has not been explored thoroughly. Furthermore, the current practical application of inflammasome inhibitors is limited to specific tumour types, hence, further studies are warranted to discover the potential of targeting the inflammasomes for the treatment of NPC.
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Ball, Daniel P., Cornelius Y. Taabazuing, Andrew R. Griswold, Elizabeth L. Orth, Sahana D. Rao, Ilana B. Kotliar, Lauren E. Vostal, Darren C. Johnson, and Daniel A. Bachovchin. "Caspase-1 interdomain linker cleavage is required for pyroptosis." Life Science Alliance 3, no. 3 (February 12, 2020): e202000664. http://dx.doi.org/10.26508/lsa.202000664.

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Pathogen-related signals induce a number of cytosolic pattern-recognition receptors (PRRs) to form canonical inflammasomes, which activate pro-caspase-1 and trigger pyroptotic cell death. All well-studied inflammasome-forming PRRs oligomerize with the adapter protein ASC (apoptosis-associated speck-like protein containing a CARD) to generate a large structure in the cytosol, which induces the dimerization, autoproteolysis, and activation of the pro-caspase-1 zymogen. However, several PRRs can also directly interact with pro-caspase-1 without ASC, forming smaller “ASC-independent” inflammasomes. It is currently thought that little, if any, pro-caspase-1 autoproteolysis occurs during, and is not required for, ASC-independent inflammasome signaling. Here, we show that the related human PRRs NLRP1 and CARD8 exclusively form ASC-dependent and ASC-independent inflammasomes, respectively, identifying CARD8 as the first canonical inflammasome-forming PRR that does not form an ASC-containing signaling platform. Despite their different structures, we discovered that both the NLRP1 and CARD8 inflammasomes require pro-caspase-1 autoproteolysis between the small and large catalytic subunits to induce pyroptosis. Thus, pro-caspase-1 self-cleavage is a required regulatory step for pyroptosis induced by human canonical inflammasomes.
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Zhang, Zhirong, Gergö Meszaros, Wan-ting He, Yanfang Xu, Helena de Fatima Magliarelli, Laurent Mailly, Michael Mihlan, et al. "Protein kinase D at the Golgi controls NLRP3 inflammasome activation." Journal of Experimental Medicine 214, no. 9 (July 17, 2017): 2671–93. http://dx.doi.org/10.1084/jem.20162040.

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The inflammasomes are multiprotein complexes sensing tissue damage and infectious agents to initiate innate immune responses. Different inflammasomes containing distinct sensor molecules exist. The NLRP3 inflammasome is unique as it detects a variety of danger signals. It has been reported that NLRP3 is recruited to mitochondria-associated endoplasmic reticulum membranes (MAMs) and is activated by MAM-derived effectors. Here, we show that in response to inflammasome activators, MAMs localize adjacent to Golgi membranes. Diacylglycerol (DAG) at the Golgi rapidly increases, recruiting protein kinase D (PKD), a key effector of DAG. Upon PKD inactivation, self-oligomerized NLRP3 is retained at MAMs adjacent to Golgi, blocking assembly of the active inflammasome. Importantly, phosphorylation of NLRP3 by PKD at the Golgi is sufficient to release NLRP3 from MAMs, resulting in assembly of the active inflammasome. Moreover, PKD inhibition prevents inflammasome autoactivation in peripheral blood mononuclear cells from patients carrying NLRP3 mutations. Hence, Golgi-mediated PKD signaling is required and sufficient for NLRP3 inflammasome activation.
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Yang, Qingrui, Chengcheng Yu, Zhaowen Yang, Qing Wei, Kun Mu, Ying Zhang, Wei Zhao, Xiaofeng Wang, Wanwan Huai, and Lihui Han. "Deregulated NLRP3 and NLRP1 Inflammasomes and Their Correlations with Disease Activity in Systemic Lupus Erythematosus." Journal of Rheumatology 41, no. 3 (December 15, 2013): 444–52. http://dx.doi.org/10.3899/jrheum.130310.

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Objective.NOD-like receptor family, pyrin domain containing 3 and 1 (NLRP3 and NLRP1) inflammasomes are molecular platforms that sense the damage or danger signals of cells. We investigated whether NLRP3/NLRP1 inflammasomes are involved in the pathogenesis and progression of systemic lupus erythematosus (SLE).Methods.Expressions of inflammasome components at the mRNA and protein levels in the peripheral blood mononuclear cells (PBMC) from patients with SLE and healthy controls were investigated by quantitative real-time transcription PCR and Western blot, respectively. Correlations between NLRP3/NLRP1 inflammasome components’ expression and clinical disease progression were investigated. Expressions of NLRP3/NLRP1 inflammasomes before and after treatment in the patients with SLE were also analyzed and compared.Results.Our data showed that expressions of NLRP3/NLRP1 inflammasomes were significantly downregulated in PBMC from patients with SLE compared with PBMC from healthy controls. Further, expressions of NLRP3/NLRP1 inflammasomes were negatively correlated with the SLE Disease Activity Index, and regular glucocorticoid treatment significantly corrected this deregulation of these inflammasomes. Further analysis showed that type I interferon (IFN) level was significantly negatively correlated with expression of NLRP3/NLRP1 inflammasomes, which indicated that enhanced IFN-I level in patients with SLE was responsible, at least to a great degree, for the deregulation of inflammasomes.Conclusion.These results indicated deregulation of NLRP3/NLRP1 inflammasomes in patients with SLE, and suggested an important role for inflammasomes in the pathogenesis and progression of SLE.
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Nourbakhsh, Fahimeh, Morgayn I. Read, George E. Barreto, and Amirhossein Sahebkar. "Astrocytes and Inflammasome: A Possible Crosstalk in Neurological Diseases." Current Medicinal Chemistry 28, no. 24 (August 13, 2021): 4972–94. http://dx.doi.org/10.2174/0929867328666210301105422.

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Inflammasome research has primarily focused on neurological tissue, particularly on damaged tissue. Most current neurological literature involves in vivo and in vitro studies utilizing astroglia, as astroglia express the cytoskeletal glial fibrillary acidic protein (GFAP), which is used as a hallmark of neuropathological disorders. Research suggests that astrocytes respond to all forms of neurological damage or disease through reactive astrogliosis. Additionally, there is a consensus among scientists that inflammasomes play an important role in neuroinflammation. This review focuses on the latest developments in inflammasome biology, describing the current understanding of how inflammasomes can be triggered in the brain and summarizing the literature on the relevance of inflammasome NLR in prevalent neurological diseases.
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Dissertations / Theses on the topic "Inflammasones"

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Schattgen, Stefan A. "Sensing of Endogenous Nucleic Acids by the Innate Immune System during Viral Infection: A Dissertation." eScholarship@UMMS, 2003. http://escholarship.umassmed.edu/gsbs_diss/764.

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Innate sensing of nucleic acids lies at the heart of antiviral host defense. However, aberrant activation of innate sensors by host nucleic acids can also lead to the development of autoimmune diseases. Such host nucleic acids can also be released from stressed, damaged or dying cells into the tissue microenvironment. It however remains unclear how the extracellular nucleic acids impacts the quality of the host immune responses against viral infections. Using a mouse model of influenza A virus (IAV) infection, we uncovered an important immune-regulatory pathway that tempers the intensity of the host-response to infection. We found that host-derived DNA from necrotic cells accumulates in the lung microenvironment during IAV infection, and is sensed by the DNA receptor Absent in Melanoma 2 (AIM2). AIM2-deficiency resulted in severe immune pathology highlighted by enhanced recruitments of immune cells, and excessive systemic inflammation after IAV challenge, which led to increased morbidity and lethality in IAV-infected mice. Interestingly, these effects of AIM2 were largely independent of its ability to mediate IL-1β maturation through inflammasome complexes. Finally, ablation of accumulated DNA in the lung by transgenic expression of DNaseI in vivo had similar effects. Collectively, our results identify a novel mechanism of cross talk between PRR pathways, where sensing of hostderived nucleic acids limits immune mediated damage to virus infected tissues.
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Schattgen, Stefan A. "Sensing of Endogenous Nucleic Acids by the Innate Immune System during Viral Infection: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/764.

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Innate sensing of nucleic acids lies at the heart of antiviral host defense. However, aberrant activation of innate sensors by host nucleic acids can also lead to the development of autoimmune diseases. Such host nucleic acids can also be released from stressed, damaged or dying cells into the tissue microenvironment. It however remains unclear how the extracellular nucleic acids impacts the quality of the host immune responses against viral infections. Using a mouse model of influenza A virus (IAV) infection, we uncovered an important immune-regulatory pathway that tempers the intensity of the host-response to infection. We found that host-derived DNA from necrotic cells accumulates in the lung microenvironment during IAV infection, and is sensed by the DNA receptor Absent in Melanoma 2 (AIM2). AIM2-deficiency resulted in severe immune pathology highlighted by enhanced recruitments of immune cells, and excessive systemic inflammation after IAV challenge, which led to increased morbidity and lethality in IAV-infected mice. Interestingly, these effects of AIM2 were largely independent of its ability to mediate IL-1β maturation through inflammasome complexes. Finally, ablation of accumulated DNA in the lung by transgenic expression of DNaseI in vivo had similar effects. Collectively, our results identify a novel mechanism of cross talk between PRR pathways, where sensing of hostderived nucleic acids limits immune mediated damage to virus infected tissues.
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Adindu, Uzowuru Cosmas. "Inflammasome : Investigating the effect of NEK7 in the activation of the NLRP3 Inflammasome." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-18937.

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Inflammation is a biological defence mechanism applied by living organisms against foreign invaders. In the response to DAMPs and PAMPs, organisms use inflammatory multi-protein complexes to fight the attackers. The most studied inflammasome proteins are NLRP3, ASC and Caspase-1. This study is aimed at understanding the role of NEK7 protein in the NLRP3 inflammasome’s activation, using CRISPR/Cas9 system. To determine the effect of CRISPR/Cas9 and transfection, mRNA expression was analyzed. The results obtained suggest that neither the transfection nor the NEK7 protein knockout have sufficiently worked. This study could not experimentally establish that NEK7 triggers NLRP3 inflammasome activation because ELISA was not conducted to verify the levels of cytokines emitted, due to there being no statistical differences between the samples. Above all, the research question in this thesis project was not answered because the instability of the ACTB reference gene negatively influenced the results. However, previous related studies conclude that NEK7 plays a crucial role in the activation of the NLRP3 inflammasome.
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Janczy, John Roger. "Mechanisms for activation and inhibition of inflammasomes." Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/1643.

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Activation of the cysteine protease caspase-1 and the subsequent processing and secretion of the pro-inflammatory cytokines IL-1Β and IL-18 is central to the inflammatory response as well as the induction of adaptive immune responses. Caspase-1 is activated as a part of a high-molecular weight multi-protein complex termed the inflammasome. The NLRP3 inflammasome is by far the best studied of these complexes, and it is the most promiscuous in terms of activating signals. The diversity of NLRP3 activating signals makes it likely that NLRP3 does not recognize each agonist directly, rather it detects a molecule that is generated, revealed, or altered by cellular stress. Recent studies have indicated that mitochondrial dysfunction is crucial for NLRP3 inflammasome activation, yet the activating ligand has not yet been identified. Appropriate and timely activation of this inflammatory pathway is required for host immunity to a variety of pathogens, however dysregulated activation leads to autoinflammation and potentially autoimmunity. Hence it is important to identify mechanisms for inflammasome activation and regulation. Therefore, this dissertation has focused on investigating the mechanisms for activation and regulation of the NLRP3 inflammasome, and the biological consequences of these changes. We show that the mitochondrial lipid cardiolipin is required for NLRP3 inflammasome activation. We have also identifying a novel mechanism by which inflammasome activation is regulated. Data presented in this dissertation shows that IgG immune complexes effectively suppress inflammasome activation and the subsequent processing and secretion of IL-1Α and IL-1Β. Furthermore we show that immunization with IgG immune complexes suppresses both Th2 and Th17 immune responses. Together these data provide novel insights into the activating and regulatory pathways of both the innate and adaptive immune systems.
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Srinivasan, 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.

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Single Nucleotide Polymorphisms (SNPs) in the intracellular pattern recognition receptor gene NLRP3 are associated with susceptibility to Crohn’s disease, a form of inflammatory bowel disease (IBD). Following cell damage or infection, NLRP3 triggers the formation of inflammasomes, a multimolecular protein complex containing NLRP3, ASC and caspase-1, which mediate secretion of IL-1β and IL-18. NLRP3 inflammasome activation in macrophages has been implicated in protection against several pathogens, but whether NLRP3 activation in tissue cells contributes to protective immunity against bacterial pathogens is unknown. We show that upon infection with the attaching/effacing (A/E) intestinal pathogen Citrobacter rodentium, Nlrp3-/- and Asc-/- mice displayed higher bacterial colonization, more weight loss and exacerbated intestinal inflammation. We further show that Nlrp3 inflammasome activation in intestinal epithelial cells (IECs) acts rapidly after infection to limit bacterial replication and penetration, and inhibits the development of inflammatory pathology in the gut. We also show that epithelial Nlrp3-mediated protection is independent of the classical inflammasome cytokines IL-1β and IL-18. Thus an Nlrp3-Asc circuit in IECs regulates early defense against a mucosal pathogen and limits inflammation in the intestine. Nlrp3 inflammasome activation has also been implicated in protection in acute models of experimental colitis, but its role in chronic models of colitis is unknown. We found that Asc signaling is necessary for the development of innate chronic intestinal inflammation driven by Helicobacter hepaticus. Thus while deficient inflammasome signaling in tissue cells increases susceptibility towards enteric pathogens, excessive inflammasome activation can drive chronic intestinal inflammation.
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Kannan, Harsha. "The Inflammasome in Acute Myocarditis." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3108.

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Acute myocarditis is an acute inflammatory syndrome characterized by myocardial damage and dysfunction often due to a viral infection followed by a variable development over time. There are currently no specific treatments and standard treatments for heart failure are generally applied. The inflammasome is a recently identified macromolecular structure that occupies a central role in the amplification of the inflammatory response and promotion of cell death during acute and chronic infections. We hypothesized the formation of the inflammasome in acute myocarditis. To investigate, samples of patients were collected from the Cardiomyopathy Registry in Trieste, with 12 cases of biopsy-proven myocarditis and 11 cases of autopsy-proven myocarditis stained for major components of the inflammasome through immunofluorescence; 10 of the 12 (83.3%) biopsy cases and 8 of the 11 (72.7%) autopsy cases presented formation of the inflammasome in a variety of cells including resident cells (i.e. cardiomyocytes, endothelial cells, fibroblasts) and infiltrating cells (i.e. leukocytes) while varying in intensity and distribution. Control samples of 5 subjects not presenting with any acute cardiac events showed no formation of the inflammasome. While further studies should look to elucidate the correlation of inflammasome-formation and progression of disease, this finding paves the way for further insight into the pathophysiology of acute myocarditis.
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Poli, Caroline. "Il-26 : une cytokine pro-inflammatoire stimulant les cellules immunitaires innées myéloïdes." Thesis, Angers, 2017. http://www.theses.fr/2017ANGE0068.

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Physiologiquement, l’ADN, séquestré dans les noyaux, n’est pas détecté par les récepteurs de danger du système immunitaire. En revanche, au cours d’inflammations chroniques, une rupture de la tolérance vis-à-vis de l’ADN du soi, consécutivement à sa libération dans le milieu extracellulaire par les cellules mortes, a été démontrée. L’accès de l’ADN extracellulaire aux récepteurs intracellulaires est médié par des molécules cargo capables de s’associer à l’ADN extracellulaire et d’induire sont internalisation.L’IL-26, qui est un membre de la famille de l’IL-10, a été décrite comme une cytokine pro-inflammatoire, dont les mécanismes moléculaires restent mal connus. Nous avons démontré que l’IL-26 se lie à l’ADN, permet son internalisation dans le cytosol des cellules myéloïdes et la sécrétion de cytokines pro inflammatoires via la voie STING et la voie des inflammasomes. La modélisation informatique de l’IL-26, basée sur la structure de l’IL-10,met en évidence des caractéristiques structurales similaires aux molécules cargo : un domaine de liaison à l’ADN, deux hélices amphipathiques et un motif d’ancrage à la membrane. De plus, des complexes circulants d’IL-26-ADN sont retrouvés dans les sérums de patients en poussée aigues de vascularite à ANCA,une pathologie inflammatoire chronique. L’IL-26 est détectée dans les lésions de glomérulonéphrite aigue nécrosante à croissants, ainsi qu’au niveau des cellules musculaires lisses artérielles de ces patients. Ces dernières sécrètent de l’IL-26 en présence de cytokinespro-inflammatoires. En conclusion, l’IL-26 établit d’une boucle d’autoamplification entre une mort cellulaire intense et l’inflammation
In physiological conditions, self-DNA released by dying cells is not detected by intracellular DNA sensors. Inchronic inflammatory disorders, unabated inflammation has been associated with a break in innate immune tolerance to self-DNA. However, to gain access to intracellular DNA sensors, extracellular DNA has to complex with DNA-binding molecules. IL-26 is a member of the IL-10 cytokine family, overexpressed in numerous chronic inflammatory diseases, which biological activity remains unclear. We demonstrate here that IL-26 binds to DNA and shuttles it in the cytosol of human myeloid cells. As a consequence, IL-26 allows extracellular DNA to trigger proinflammatory cytokine secretion by monocytes, in a STING- and inflammasome-dependent manner. Supporting these biological properties, IL-10-based modelling predicts two DNA-binding domains, two amphipathic helices, and an in-plane membrane anchor in IL-26, structural features of cationic amphipathic cell penetrating peptides. In line with these properties, patients with active autoantibody-associated vasculitis, a chronic relapsing autoimmune inflammatory disease associated with extensive cell death, exhibit high levels of both circulating IL-26 and IL-26-DNA complexes. Moreover, in patients with crescentic glomerulonephritis, IL-26 is expressed by renal arterial smooth muscle cells and deposits in necrotizing lesions. Accordingly, human primary smooth cells secrete IL-26 in response to proinflammatory cytokines. In conclusion, IL-26 expressed in lesions confers proinflammatory properties to DNA released by dying cells, setting up a positive amplification loop between extensive cell death and unabated inflammation
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de, Almeida Pereira Milton César. "Inflammasome signalling during Salmonella Typhimurium infection." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/283642.

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The innate immune system is the first line of defence against infection. It is comprised of physicochemical barriers and a variety of cell types including macrophages and dendritic cells. Pathogens express specific pathogen associated molecular patterns (PAMP) which are recognised by pattern recognition receptors (PRR) on macrophages to initiate an innate immune response. Gram-negative bacteria such as Salmonella enterica serovar Typhimurium express a range of bacterial PAMPs recognised by Toll-like receptors (TLRs) including lipopolysaccharides (LPS) recognised by TLR-4 and lipoproteins by TLR-2. The activation of TLRs results in activation of nuclear factor κB (NF-κB) to drive transcription of mRNA coding for pro-inflammatory proteins such as tumor necrosis factor α (TNF-α) and pro-interleukin (IL) 1β. Myeloid cells also possess intracellular PRRs including the nucleotide-binding domain and leucine-rich repeat (NLR) family. NLR family CARD domain- containing protein 4 (NLRC4) and NLR family pyrin domain-containing protein 3 (NLRP3) are the main NLRs engaged in recognising S. Typhimurium infection, leading to formation of the inflammasome. The inflammasome is a macromolecular complex assembled in the cytoplasm, and usually contains a NLR, the structural protein apoptosis-associated speck-like protein containing a CARD (ASC) and effector enzymes such as cysteine-dependent aspartate-directed protease (caspase) -1 and caspase-8. This structure is responsible for processing the cytokines pro- IL-1β and pro-IL-18 to their mature form and is involved in triggering a pro-inflammatory process of cell death termed pyroptosis. The formation of the inflammasome therefore results in cell death and secretion of proinflammatory cytokines which play important roles in controlling infections. Inflammasome activity must be tightly coordinated, as its dysregulation is associated with a variety of auto-inflammatory and auto-immune diseases. The signalling events leading to inflammasome assembly are poorly understood and the molecules involved in fine-tuning its activity are only beginning to be discovered. The aim of this thesis was to discover new molecules involved in inflammasome activation and/or in keeping its activity in check. To achieve this goal, I performed S. Typhimurium infection assays in primary bone marrow derived macrophages (BMDM) derived from C57BL/6 mice wild type (WT) and compared the resulting cellular viability, intracellular bacteria counts and IL-1β production to that of BMDMs derived from C57BL/6 mice lacking proteins involved with, or suspected to be involved with, innate immune activity. Amongst the proteins I studied, caspase recruitment domain 9 (CARD9) inhibited inflammasome-mediated IL-1β production. Multiple independent genome-wide association studies link this protein to inflammatory pathologies such as Crohn's disease, but its role in canonical inflammasomes was largely unexplored. To investigate how CARD9 inhibits inflammasome-mediated IL-1β production I have conducted assays in WT and Card9-/- BMDMs, including stimulation of specific NLRs with their purified ligands, infection with bacterial strains deficient in NLRC4 activation, and infection assays in presence of pharmacological inhibitors. By employing these approaches, I observed that CARD9 has a negative role on NLRP3-dependent IL-1β production. Specifically, in response to activation of the NLRP3 by Salmonella infection, CARD9 negatively regulates pro-IL-1β transcription, and decreases IL-1β processing by inhibiting spleen tyrosine kinase (SYK)-mediated NLRP3 activation and represses caspase-8 activity in the inflammasome. CARD9 expression is suppressed in the course of S. Typhimurium infection which may act as a mechanism to increase IL-1β production during the infection. In conclusion, I have established a connection between CARD9 and IL-1β production by the canonical NLRP3 inflammasome and elucidated some of the mechanisms involved in this process. I have also found evidence that other proteins are likely to be involved in inflammasome regulation and the elucidation of their roles will be addressed in future studies.
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Palazón, Pablo. "Mechanisms and consequences of inflammasome activation." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/mechanisms-and-consequences-of-inflammasome-activation(995047bf-afce-496f-86be-efb0034ad490).html.

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Inflammation is the response of the body to injury or threats. Immune cells such as macrophages have a crucial role in controlling and regulating this process. The potent pro-inflammatory cytokines interleukin (IL)-1beta and IL-18 are synthesized by macrophages as inactive precursors which activation follows a unique mechanism involving the activation of caspase-1 by assembly of a macromolecular complex called the inflammasome. However, the assembly of the inflammasome is a double-edged sword. Although inflammasome activation is necessary for a normal inflammatory response, its malfunction can trigger and contribute to inflammatory disorders such as gout, arthritis or cryopirin-associated periodic syndromes (CAPS). The fine regulation of this mechanism and the cell death associated with it is key for the outcome of the inflammatory process. In this thesis we tackle three aspects of the mechanisms and consequences of inflammasome activation. First we studied the role of the deubiquitinases USP7 and USP47 in inflammasome activation. We showed how USP7 and USP47 activity is increased upon danger signals and how that is necessary for the assembly of the inflammasome. We also pointed how their inhibition dampens the deubiquitination of ASC using a BRET2 assay. Second we examined how the activity of IL-18 is controlled by the release of IL-18BP during inflammasome activation. We showed how IL-18BP release increased upon membrane permeabilization and pyroptosis. This release happens in other types of lytic cell (necrosis and necroptosis) death but not in apoptosis. Finally, we showed that this IL-18BP acute release dampens IL-18 signalling and IFN gamma production by PBMCs. These results demonstrate a novel mechanism by which lytic cell death could dampen IL-18-driven inflammation and highlights a key role for IL-18BP in inflammasome related diseases. Finally we studied the role of inflammasome in lung epithelial cells as a model to investigate lung infections. We found that lung epithelial cells lack NLRP3 inflammasome activity and components, but express caspase-4 and caspase-8 which could have a role in the release of IL-1 family of cytokines. To conclude we showed how lung epithelial release IL-18 upon Aspergillus fumigatus infection. Overall, this thesis enhances our understanding of the mechanisms that control IL-1beta and IL-18 activity by regulating inflammasome activation and by understanding the consequences of its activation.
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Cirelli, Kimberly M. "Rodent inflammasome activation by Toxoplasma gondii." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/105635.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.
Cataloged from PDF version of thesis.
Includes bibliographical references.
Toxoplasma gondii is an obligate intracellular pathogen capable of chronically infecting nearly all warm-blooded animals, including humans. The chronic stage is characterized by the presence of semi-dormant cysts in brain and muscle tissues. These cysts are crucial in the success of Toxoplasma as they are orally infectious and allow for the transmission of the parasite between hosts. As the host immune response drives cyst formation, the establishment of this chronic infection relies on the parasite's ability to find a balance between activation of a host immune response and evasion of parasiticidal mechanisms. This balance is achieved through the modulation of host cell processes by parasite proteins secreted from specialized secretory organelles known as rhoptries and dense granules. Here, we report that Toxoplasma activates the inflammasomes in mice and rats. The inflammasomes are a set of cytoplasmic pattern recognition receptors (PRRs). Activation of the inflammasomes results in caspase-1 activation and the cleavage and release of the pro-inflammatory cytokines, Interleukin (IL)-1[beta] and IL-18. IL-1p is an important mediator of local inflammation and neutrophil recruitment. IL- 18 induces Interferon (IFN)-[gamma], which is a critical cytokine in the control of Toxoplasma. A form of cell death, termed pyroptosis, can accompany inflammasome activation. The NLRP3 inflammasome is activated in mouse macrophages, leading to the secretion of IL-1[beta] in vitro. The NLRP1 and NLRP3 inflammasomes play a major role in mouse survival and control of parasite replication in vivo. The NLRPI inflammasome is activated in infected macrophages from rats that are able to completely clear infection. Toxoplasma infection leads to the secretion of active IL-I[beta] and IL-18. Activation of the NLRP1 inflammasome leads to pyroptosis, a programmed form of cell death. Pyroptosis prevents parasite replication within the host cell and likely promotes clearance by nearby immune cells. Using a chemical mutagenesis screen, we identified three Toxoplasma dense granule proteins (GRAs), GRA18, GRA27 and GRA28, essential for NLRP1 inflammasome activation and pyroptosis in rat macrophages. Our work has identified Toxoplasma gondii as a novel activator of the rodent inflammasomes and demonstrated host cell death as a mechanism to control parasite replication. We have also identified three novel parasite proteins required for this activation, providing insight into interactions between parasite and host, which may aid in the treatment of human infection.
by Kimberly M. Cirelli.
Ph. D.
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Books on the topic "Inflammasones"

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Couillin, Isabelle, Virginie Pétrilli, and Fabio Martinon, eds. The Inflammasomes. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5.

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Couillin, Isabelle. The Inflammasomes. Basel: Springer Basel AG, 2011.

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De Nardo, Christine M., and Eicke Latz, eds. The Inflammasome. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-523-1.

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Cordero, Mario D., and Elísabet Alcocer-Gómez, eds. Inflammasomes: Clinical and Therapeutic Implications. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-89390-7.

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Nardo, Christine De, and Eicke Latz. The inflammasome: Methods and protocols. New York: Humana Press, 2013.

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Backert, Steffen, ed. Inflammasome Signaling and Bacterial Infections. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41171-2.

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Couillin, Isabelle, Virginie Pétrilli, and Fabio Martinon. The Inflammasomes. Springer, 2013.

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DNA Sensors and Inflammasomes. Elsevier, 2019. http://dx.doi.org/10.1016/s0076-6879(19)x0011-7.

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Inflammasomes: Clinical and Therapeutic Implications. Springer, 2019.

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Cordero, Mario D., and Elísabet Alcocer-Gómez. Inflammasomes: Clinical and Therapeutic Implications. Springer, 2018.

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Book chapters on the topic "Inflammasones"

1

Girardis, M., S. Busani, and S. De Biasi. "Immune System Dysfunction and Multidrug-resistant Bacteria in Critically Ill Patients: Inflammasones and Future Perspectives." In Annual Update in Intensive Care and Emergency Medicine, 105–12. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13761-2_8.

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Inoue, Makoto, Masashi Kanayama, and Mari L. Shinohara. "Inflammasomes." In Encyclopedia of Inflammatory Diseases, 1–15. Basel: Springer Basel, 2013. http://dx.doi.org/10.1007/978-3-0348-0620-6_77-1.

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Inoue, Makoto, Masashi Kanayama, and Mari L. Shinohara. "Inflammasomes." In Compendium of Inflammatory Diseases, 619–33. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_77.

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Pétrilli, Virginie, and Fabio Martinon. "Molecular Definition of Inflammasomes." In The Inflammasomes, 1–16. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_1.

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Apetoh, Lionel. "Cancer, Inflammasomes, and Adjuvanticity." In The Inflammasomes, 151–63. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_10.

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Ryffel, Bernhard, Dieudonnée Togbe, and Isabelle Couillin. "Inflammasome and Lung Pathologies." In The Inflammasomes, 165–82. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_11.

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Gattorno, Marco, and Anna Rubartelli. "Mechanisms of NLRP3 Inflammasome Activation in CAPS Patients." In The Inflammasomes, 183–95. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_12.

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Hernandez, Juan-Carlos, Cherilyn M. Sirois, and Eicke Latz. "Activation and Regulation of the NLRP3 Inflammasome." In The Inflammasomes, 197–208. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_13.

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Labbé, Katherine, and Maya Saleh. "Pyroptosis: A Caspase-1-Dependent Programmed Cell Death and a Barrier to Infection." In The Inflammasomes, 17–36. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_2.

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Ulland, Tyler K., and Fayyaz S. Sutterwala. "Activation of the Inflammasome by Bacterial Pathogens." In The Inflammasomes, 37–50. Basel: Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0348-0148-5_3.

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Conference papers on the topic "Inflammasones"

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Cox Jr, Ruan, Amanda Hodgkins, Prasanna Tamarapu Parthasarathy, Michelle Kaminsky, Rajan Babu Venugopal, Jutaro Fukumoto, Itsuko Fukumoto, Richard Lockey, and Narasaiah Kolliputi. "Resolvin Inhibits The Cryopyrin/Nalp3 Inflammasome." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1428.

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Exline, Matthew C., Anasuya Sarkar, Beth Y. Besecker, Jennifer L. Hollyfield, Srabani Mitra, and Mark D. Wewers. "Inflammasome Constituents Released Via Microvesicles During Sepsis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1378.

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SHAIK, RAHAMTHULLA, Narasaiah Kolliputi, and Aaron B. Waxman. "Activation Of Inflammasome In Pulmonary Arterial Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4865.

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Shin, Jin Na, Elmoataz A. H. Abdel Fattah, Soyoung Ko, and N. T. Eissa. "Altered Proteastasis In Macrophages Induces Inflammasome Activation." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1966.

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Stübke, K., J. Büter, and C. Rudack. "Role of the inflammasomes in the development of polyposis nasi." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640920.

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Thompson, Joyce K., Maximilian B. MacPherson, Stacie L. Beuschel, and Arti Shukla. "Abstract 3164: Inflammasomes: fanning the flames of malignant mesothelioma initiation." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3164.

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Reichel, C., L. Mittmann, J. Schaubächer, K. Lauber, F. Krombach, M. Canis, and B. Uhl. "The NLRP3 inflammasome regulates neutrophil trafficking to HNSCC." In Abstract- und Posterband – 89. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Forschung heute – Zukunft morgen. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1640141.

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Graustein, A., W. R. Berrington, K. J. Buckingham, F. K. Nguyen, L. L. Joudeh, M. J. Bamshad, R. L. Gibson, T. R. Hawn, and M. J. Emond. "The NLRP3 Inflammasome in the Cystic Fibrosis Macrophage." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2660.

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Sorrentino, Rosalinda, Michela Terlizzi, Pasquale Imitazione, Chiara Colarusso, Maria D'Amato, Alessandro Vatrella, Aldo Pinto, and Antonio Molino. "Role of the inflammasome in idiopathic pulmonary fibrosis." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa2027.

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Samara, Katerina D., Ismini Lasithiotaki, Eliza Tsitoura, Ioannis Giannarakis, Anna Psaraki, Eleni Bibaki, Irini Lambiri, Nikolaos Siafakas, and Katerina M. Antoniou. "Lung cancer immune cells exhibit inhibited inflammasome response." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa530.

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Reports on the topic "Inflammasones"

1

Testa, Joseph R. Role of the Inflammasome in Asbestos-Induced Mesothelioma Formation. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada570536.

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Schmitz, Karl R. Regulation of the Inflammasome, a Modulator of Caspase-Mediated Cytokine Production. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada488588.

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Schmitz, Karl. Regulation of the Inflammasome, a Modulator of Caspase-1 Mediated Cytokine Production. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada517127.

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Schmitz, Karl R. Regulation of the Inflammasome, a Modulator of Caspase-1 Mediated Cytokine Production. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada509759.

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