Relevant bibliographies by topics / Il-33 vih

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Il-33 vih'

Author: Grafiati
Published: 25 May 2024
Last updated: 31 July 2025

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Journal articles on the topic "Il-33 vih"

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S, Traoré. "Survie des personnes vivant avec le VIH et le Sida suivies dans les 17 sites de traitement antirétroviral au Mali." Mali Santé Publique 10, no. 02 (2021): 44–49. http://dx.doi.org/10.53318/msp.v10i02.1796.

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Introduction : Au Mali, malgré de nombreuses campagnes de prévention et de l'efficacité de la thérapie antirétrovirale, les cas de décès liés au VIH touchent beaucoup plus les couches productives. Pour mieux élucider ce constat nous avons étudié la survie des Personnes Vivant avec le VIH suivies pendant 5 ans au Mali. Matériel et méthodes : Il s'agissait d'une étude de cohorte, incluant 39619 personnes vivant avec le VIH suivis pendant 5 ans sur les 17 sites d'ESOPE du Mali. Les données collectées concernent celles des années 1999 à 2014, elles ont été analysées par le logiciel STATA version 1
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Keita, BB, and Et Al. "Facteurs associés au décès des personnes infectées par le virus de l’immunodéficience humaine sous traitement antirétroviral au Centre Walé de Ségou, Mali." Revue Malienne d'Infectiologie et de Microbiologie 18, no. 2 (2024): 38–49. http://dx.doi.org/10.53597/remim.v18i2.2733.

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Introduction : Bien que le rôle des facteurs cliniques/biologiques associés à la mortalité ait déjà été exploré chez les patients séropositifs. Cependant, peu d'attention a été accordée jusqu'à présent à l'impact potentiel de l'absence de soutien psychosocial sur la mortalité chez les PV VIH. L'objectif de ce travail était d'étudier non seulement les facteurs clinico-biologiques mais aussi l'impact du manque de soutien psychosocial sur la mortalité des patients atteints du VIH. Méthode et Matériels : Il s’agissait d’une étude de cohorte. La durée de suivi était de 5 ans (2017 à 2021). La colle
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Abdourahimi, D., D. Yehadji, E. Briskin, et al. "Facteurs associés à la létalité chez les patients hospitalisés pour le VIH avancé." Public Health Action 13, no. 2 (2023): 19–24. http://dx.doi.org/10.5588/pha.23.0009.

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CONTEXTE : Une unité soutenue par Médecins Sans Frontières (MSF) qui prend en charge les patients avec un VIH avancé à l’Hôpital National de Donka, Conakry, Guinée.OBJECTIF : Déterminer les facteurs liés à la survenue du décès chez les patients hospitalisés dans l’unité entre 2017 et 2021.SCHÉMA : Ceci est une analyse rétrospective de données de routine des patients hospitalisés pour le VIH avancé.RÉSULTATS : Au total, 3,718 patients étaient inclus, d’âge médian de 40 ans (IQR 33–51), dont 2,241 (60,3%) femmes. Le taux de moyen de décès était de 33,6% (n = 1,240). Il était passé de 40% en 2017
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Beye, SA, and Et Al. "Prévalence des infections nosocomiales au Centre Hospitalier Universitaire du Point G de Bamako, Mali." Revue Malienne d'Infectiologie et de Microbiologie 19, no. 1 (2024): 45–49. http://dx.doi.org/10.53597/remim.v19i1.2794.

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Objectifs de cette étude était de déterminer la prévalence hospitalière des infections nosocomiales. Patients et méthodes : Il s’agissait d’une étude prospective transversale descriptive sur une période de six (6) semaines. Résultats : 463 patients ont séjourné pendant au moins 48 heures. Parmi eux, 57 patients inclus soit une prévalence de 12,3%. L’âge moyen était de 45,4 ± 20,8 ans. La durée moyenne du séjour était de 21,7 ± 12,7 jours. Les patients provenaient de la réanimation (17,5%), la médecine interne et la neurologie dans 15,8% chacune. L’immunodépression au VIH a été retrouvée dans 1
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Usman, S. O., O. M. Ajayi, O. Ebiekura, N. Egbonrelu, G. Ebhojie, and A. O. Ariyo. "Evidence of virological failure in patients on second-line anti-retroviral therapy in Southwestern Nigeria: An indication for HIV drug resistance testing." African Journal of Clinical and Experimental Microbiology 22, no. 3 (2021): 415–19. http://dx.doi.org/10.4314/ajcem.v22i3.13.

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Background: In sub-Saharan Africa where genotypic anti-retroviral (ARV) drug resistance testing is rarely performed and poor adherence is blamed for the inability to achieve viral suppression and treatment failure, programmatic approaches to preventing and handling these are essential. This study was aimed at assessing the virological outcomes among HIV patients receiving second-line anti-retroviral therapy (ART) in Southwestern Nigeria.Methodology: This was a 5-year observational retrospective study of randomly selected people living with HIV (PLWHIV) who have been switched to second-line ART
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Mathias, Clinton B., Jeffrey Rovatti, and Stephanie Polukort. "IL-10 enhances IgE-independent IL-33-mediated mast cell cytokine production." Journal of Immunology 198, no. 1_Supplement (2017): 145.8. http://dx.doi.org/10.4049/jimmunol.198.supp.145.8.

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Abstract IgE antibodies play a critical role in antigen-mediated mast cell activation. However, mast cells can be activated via IgE-independent mechanisms including signaling via the IL-33 receptor ST2. We have previously shown that the Th2-derived cytokine IL-10 can enhance IgE-dependent mucosal mast cell activation and promote mast cell function and survival. However, whether the effects of IL-10 on mast cells are global in nature and not limited to IgE-mediated signaling is not clear. To determine whether IL-10 can prime the activation of mast cells mediated by IgE-independent signals such
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Miller, Ashley M., Damo Xu, Darren L. Asquith, et al. "IL-33 reduces the development of atherosclerosis." Journal of Experimental Medicine 205, no. 2 (2008): 339–46. http://dx.doi.org/10.1084/jem.20071868.

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Atherosclerosis is a chronic inflammatory disease of the vasculature commonly leading to myocardial infarction and stroke. We show that IL-33, which is a novel IL-1–like cytokine that signals via ST2, can reduce atherosclerosis development in ApoE−/− mice on a high-fat diet. IL-33 and ST2 are present in the normal and atherosclerotic vasculature of mice and humans. Although control PBS-treated mice developed severe and inflamed atherosclerotic plaques in the aortic sinus, lesion development was profoundly reduced in IL-33–treated animals. IL-33 also markedly increased levels of IL-4, -5, and -
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Park, Su-Ho, Myun Soo Kim, Hui Xuan Lim, Daeho Cho та Tae Sung Kim. "IL-33-matured dendritic cells promote Th17 cell responses via IL-1β and IL-6". Cytokine 99 (листопад 2017): 106–13. http://dx.doi.org/10.1016/j.cyto.2017.07.022.

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Huang, Lu, Congcong Fu, Sha Liao, and Youming Long. "IL-33 relieves nerve injury by mediating microglial polarization in neuromyelitis optica spectrum disorders via the IL-33/ST2 pathway." IBRO Neuroscience Reports 17 (December 2024): 177–87. http://dx.doi.org/10.1016/j.ibneur.2024.07.008.

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Tsuji, Gaku, Akiko Hashimoto-Hachiya, Vu Hai Yen, et al. "Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1." Journal of Clinical Medicine 9, no. 3 (2020): 891. http://dx.doi.org/10.3390/jcm9030891.

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Background: IL-33, one of the IL-1 superfamily cytokines, has been shown to be associated with pruritus and inflammation in atopic dermatitis (AD). Furthermore, IL-33 production derived from keratinocytes reportedly has a crucial role in the development of AD; however, the mechanism of IL-33 expression has not been fully understood. Methods: We analyzed IL-33 expression in normal human epidermal keratinocytes (NHEKs) treated with IL-4. Results: IL-4 induced the upregulation of IL-33 expression in NHEKs. Based on the findings 1) that ovo-like 1 (OVOL1), a susceptible gene of AD, upregulates fil
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Dissertations / Theses on the topic "Il-33 vih"

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Tariq, Mubashira. "IL-33/ST2 and tissue Treg/AREG pathways in the pathophysiology of HIV infection." Electronic Thesis or Diss., Paris 12, 2021. http://www.theses.fr/2021PA120017.

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Depuis les thérapies antirétrovirales (ART), les principales causes de mortalité et de morbidité sont liées à des pathologies non liées aux SIDA qui sont dûes à un niveau d’inflammation chronique de bas bruit. Cette inflammation est liée entre autre à la persistance de la perte d’homéostasie intestinale qui conduit à des translocations microbiennes dans la circulation systémique. En effet, les sujets traités et infectés par le VIH présentent une déplétion sévère et massive des lymphocytes T CD4+, en particulier dans le tissu lymphoïde associé à l'intestin (GALT) une altération de la barrière é
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Michaudel, Chloé. "Pollution à l'ozone : maintien de la barrière pulmonaire via l'IL-33, implication des autres membres de la famille IL-1 et régulation cytokinique via AhR." Thesis, Orléans, 2017. http://www.theses.fr/2017ORLE2040.

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L’ozone est un des polluants présents dans l’air que nous respirons. Les pics de ce polluant entrainent une augmentation des hospitalisations et des cas d’exacerbations d’asthme allergique. L’objectif de ce travail est d’étudier plus en détails les mécanismes inflammatoires mis en place après exposition à l’ozone. Cette étude s’est déroulée en trois axes, les deux premiers traitant du rôle de deux alarmines, l’IL-33 et l’IL-1α et le troisième se focalisant sur AhR, un récepteur impliqué dans la réponse à de nombreux polluants. Pour ce faire, des souris ont été exposées à l’ozone selon deux mod
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Arima, Hiroshi. "B cells with aberrant activation of Notch1 signaling promote Treg and Th2 cell-dominant T cell responses via IL-33." Kyoto University, 2019. http://hdl.handle.net/2433/236612.

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Book chapters on the topic "Il-33 vih"

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Cannizzaro, Francesco. "Gli errores (meta)letterari del Meandro da Augusto ai Flavi." In Studi e ricerche del Dipartimento di Lettere e Filosofia. Società Editrice Fiorentina, 2024. http://dx.doi.org/10.35948/dilef/978-88-6032-734-5.11.

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Il Meandro, fiume tortuoso per antonomasia tanto da dare il suo nome a un tipo di decorazione assai diffuso nell’arte greco-romana, in età augustea assume talora valore metaletterario sia come garanzia di epicità, a motivo del suo legame con il labirinto e l’antica Troia, sia viceversa come modello di una poetica “erratica”, metamorfica e vicina al polo dell’elegia. In questo contributo saranno brevemente analizzati e commentati in tal senso alcuni testi di Virgilio (Aen. V 250-251), Ovidio (met. VIII 159- 168; epist. IX 55-58) e Properzio (II 34, 33-40); sarà, infine, considerata la fortuna (
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Olsen Ingar and Singhrao Sim K. "Inflammasome Involvement in Alzheimer's Disease." In Advances in Alzheimer’s Disease. IOS Press, 2017. https://doi.org/10.3233/978-1-61499-706-1-17.

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Inflammasomes are responsible for the maturation of pro-inflammatory cytokines such as interleukin (IL)-1&bgr;, IL-18, and IL-33 and activation of inflammatory cell death, pyroptosis. They assemble in response to cellular infection and stress or to tissue damage, promote inflammatory reactions, and are important in regulating innate immunity particularly by acting as platforms for activation of caspase proteases. They appear to be involved in several pathological processes activated by microbes including Alzheimer's disease (AD). Best characterized in microbial pathogenesis is the nucleoti
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Asim, Muhammad, Aleena Altaf, Aamir Sohail, et al. "Perspective Chapter: Targeting PTP1B for the Treatment of Steatosis – Insights from Viscosol’s Role in Insulin-Mediated Lipid Metabolism Regulation." In Steatosis - Causes and Treatment [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1011551.

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Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as nonalcoholic fatty liver disease (NAFLD), involves excessive fat buildup in liver cells and is closely linked to insulin resistance, type 2 diabetes mellitus (T2DM), and dyslipidemia. This chapter discusses MASLD pathophysiology, focusing on disrupted lipid metabolism, inflammation, and the key role of protein tyrosine phosphatase 1B (PTP1B) in insulin signaling and metabolic balance. The high-fat diet (HFD) plus low-dose streptozotocin (STZ) mouse model mimics human T2DM and MASLD, showing hyperglycemia, lip
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Conference papers on the topic "Il-33 vih"

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Kearley, J., TJ Burwell, E. Benjamin, et al. "IL-33 Induces Airway Hyperresponsiveness and Alternative Macrophage Activation Via an IL-13 Dependent Mechanism." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2254.

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Dienger, Krista M., DeBroski Herbert, Rena Rani, et al. "Trefoil Factor 2 Mediates IL-13-Induced Allergic Asthma Via IL-33 Specific Th2 Initiation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4270.

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Upham, John, Lisa Jurak, and Yang Xi. "IL-33 augments rhinovirus-induced type 2 immune responses in asthma via selective upregulation of one chain of the IL-33 receptor." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa567.

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Maruoka, S., S. Yamada, R. Ito, et al. "A Humanized Mouse Model to Study Asthmatic Airway Inflammation Via Human IL-33/IL-13 Axis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2902.

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Scott, I. C., E. England, D. G. Rees, et al. "Tozorakimab: a dual-pharmacology anti-IL-33 antibody that inhibits IL-33 signalling via ST2 and RAGE/EGFR to reduce inflammation and epithelial dysfunction." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2467.

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Sperling, Anne I., Bryan S. Clay, Jesse Williams, Tiara Byrd, and Melissa Y. Tjota. "Dendritic Cells Produce IL-33 When Stimulated Via FcgR And TLR-4." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4271.

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Strickson, S., K. F. Houslay, V. A. Negri, et al. "Oxidised IL-33 signals via RAGE/EGFR to drive a COPD-associated phenotype." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2482.

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Xue, Lingna, Wenjing Yang, Junjie Wen, et al. "IL-33 substantially initiates and promotes EGPA development via alteration in pulmonary immune microenvironments." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.pa428.

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Man, L. H. "IL-33/ST2 Regulates Tissue Remodeling Via MAPK and NF-κB Pathways in Nasal Polyp". У American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a7177.

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Draijer, Christina, Machteld N. Hylkema, Catherine M. Greene, et al. "Estrogen Protects Against Airway Inflammation Via Upregulation Of Secretory Leukoprotease Inhibitor And Downregulation Of IL-33." 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.a6483.

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