Relevant bibliographies by topics / IL-15Rα

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  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'IL-15Rα'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "IL-15Rα"

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Burkett, Patrick R., Rima Koka, Marcia Chien, Sophia Chai, David L. Boone, and Averil Ma. "Coordinate Expression and Trans Presentation of Interleukin (IL)-15Rα and IL-15 Supports Natural Killer Cell and Memory CD8+ T Cell Homeostasis." Journal of Experimental Medicine 200, no. 7 (September 27, 2004): 825–34. http://dx.doi.org/10.1084/jem.20041389.

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The high affinity interleukin (IL)-15 receptor, IL-15Rα, is essential for supporting lymphoid homeostasis. To assess whether IL-15Rα's role in vivo is to trans present IL-15, we generated mixed bone marrow chimera from IL-15Rα– and IL-2/15Rβ–deficient mice. We find that IL-15Rα–competent, IL-2/15Rβ–deficient cells are able to support IL-15Rα–deficient natural killer (NK) and memory CD8+ T cells, thus ruling out secondary signals on these cells and demonstrating that IL-15Rα–mediated presentation of IL-15 in trans is the primary mechanism by which IL-15Rα functions in vivo. Surprisingly, using IL-15– and IL-15Rα–deficient mixed chimera, we also find that IL-15 and IL-15Rα must be expressed by the same cells to present IL-15 in trans, indicating that IL-15Rα is required on a cellular level for the elaboration of IL-15. These studies indicate that IL-15Rα defines homeostatic niches for NK and memory CD8+ T cells by controlling both the production and the presentation of IL-15 in trans to NK and CD8+ memory T cells.
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Loro, Emanuele, Erin L. Seifert, Cynthia Moffat, Freddy Romero, Manoj K. Mishra, Zheng Sun, Predrag Krajacic, et al. "IL-15Rα is a determinant of muscle fuel utilization, and its loss protects against obesity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 8 (October 15, 2015): R835—R844. http://dx.doi.org/10.1152/ajpregu.00505.2014.

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IL-15Rα is the widely expressed primary binding partner for IL-15. Because of the wide distribution in nonlymphoid tissues like skeletal muscle, adipose, or liver, IL-15/IL-15Rα take part in physiological and metabolic processes not directly related to immunity. In fast muscle, lack of IL-15Rα promotes an oxidative switch, with increased mitochondrial biogenesis and fatigue resistance. These effects are predicted to reproduce some of the benefits of exercise and, therefore, improve energy homeostasis. However, the direct effects of IL-15Rα on metabolism and obesity are currently unknown. We report that mice lacking IL-15Rα (IL-15Rα−/−) are resistant to diet-induced obesity (DIO). High-fat diet-fed IL-15Rα−/− mice have less body and liver fat accumulation than controls. The leaner phenotype is associated with increased energy expenditure and enhanced fatty acid oxidation by muscle mitochondria. Despite being protected against DIO, IL-15Rα−/− are hyperglycemic and insulin-resistant. These findings identify novel roles for IL-15Rα in metabolism and obesity.
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Mortier, Erwan, Tammy Woo, Rommel Advincula, Sara Gozalo, and Averil Ma. "IL-15Rα chaperones IL-15 to stable dendritic cell membrane complexes that activate NK cells via trans presentation." Journal of Experimental Medicine 205, no. 5 (May 5, 2008): 1213–25. http://dx.doi.org/10.1084/jem.20071913.

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Natural killer (NK) cells are innate immune effectors that mediate rapid responses to viral antigens. Interleukin (IL)-15 and its high affinity IL-15 receptor, IL-15Rα, support NK cell homeostasis in resting animals via a novel trans presentation mechanism. To better understand how IL-15 and IL-15Rα support NK cell activation during immune responses, we have used sensitive assays for detecting native IL-15 and IL-15Rα proteins and developed an assay for detecting complexes of these proteins. We find that IL-15 and IL-15Rα are preassembled in complexes within the endoplasmic reticulum/Golgi of stimulated dendritic cells (DCs) before being released from cells. IL-15Rα is required for IL-15 production by DCs, and IL-15 that emerges onto the cell surface of matured DCs does not bind to neighboring cells expressing IL-15Rα. We also find that soluble IL-15–IL-15Rα complexes are induced during inflammation, but membrane-bound IL-15–IL-15Rα complexes, rather than soluble complexes, support NK cell activation in vitro and in vivo. Finally, we provide in vivo evidence that expression of IL-15Rα specifically on DCs is critical for trans presenting IL-15 and activating NK cells. These studies define an unprecedented cytokine–receptor biosynthetic pathway in which IL-15Rα serves as a chaperone for IL-15, after which membrane-bound IL-15Rα–IL-15 complexes activate NK cells via direct cell–cell contact.
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Anderson, Barbara G., and LeBris S. Quinn. "Free IL-15 Is More Abundant Than IL-15 Complexed With Soluble IL-15 Receptor-α in Murine Serum: Implications for the Mechanism of IL-15 Secretion." Endocrinology 157, no. 3 (January 26, 2016): 1315–20. http://dx.doi.org/10.1210/en.2015-1746.

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Abstract IL-15 is a cytokine that is part of the innate immune system, as well as a proposed myokine released from skeletal muscle during physical exercise that mediates many of the positive physiological effects of exercise. Many of the immune functions of IL-15 are mediated by juxtacrine signaling via externalized IL-15 bound to membrane-associated IL-15 receptor-α (IL-15Rα). Serum and plasma samples also contain measurable concentrations of IL-15, believed to arise from proteolytic cleavage of membrane-associated IL-15/IL-15Rα complexes to generate soluble IL-15/IL-15Rα species. Here, we validate commercial assays that can distinguish the free form of IL-15 and IL-15/IL-15Rα complexes. These assays showed that most (86%) IL-15 in mouse serum resides in the free state, with a minor proportion (14%) residing in complex with IL-15Rα. Given the much shorter half-life of free IL-15 compared with IL-15/IL-15Rα complexes, these findings cast doubt on the currently accepted model for IL-15 secretion from cleavage of membrane-bound IL-15/IL-15Rα and suggest that IL-15 is released as a free molecule by an unknown mechanism.
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Lodolce, James P., Patrick R. Burkett, David L. Boone, Marcia Chien, and Averil Ma. "T Cell–Independent Interleukin 15rα Signals Are Required for Bystander Proliferation." Journal of Experimental Medicine 194, no. 8 (October 15, 2001): 1187–94. http://dx.doi.org/10.1084/jem.194.8.1187.

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Cytokine driven or “bystander” proliferation of T cells occurs in vivo independently of major histocompatibility complex–T cell receptor interactions. This process may be important for supporting T cell homeostasis and facilitating T cell responses to microbial antigens, and may involve the cytokine interleukin (IL)-15. In this study, we find that IL-15Rα–deficient (IL-15Rα−/−) mice fail to undergo poly I:C or IL-15 driven bystander proliferation of CD8+ T cells. Surprisingly, IL-15Rα−/− CD8+ T cells proliferate in response to poly I:C when adoptively transferred into normal mice, and normal CD8+ T cells fail to proliferate in IL-15Rα−/− mice. Normal mice reconstituted with IL-15Rα−/− bone marrow cells also fail to exhibit bystander responses. Thus, CD8+ T cell independent IL-15Rα signals from radiation sensitive hematopoietic cells are likely required for bystander responses. Moreover, normal CD8+ T cells proliferate in IL-15Rα−/− mice after treatment with IL-15. Therefore, IL-15Rα signals may mediate a positive feedback loop involving the further physiological production of IL-15. These findings provide new insights into how IL-15Rα supports memory phenotype CD8+ T cell proliferation, and suggest novel mechanisms by which memory CD8+ T cells are maintained in vivo.
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Koka, Rima, Patrick R. Burkett, Marcia Chien, Sophia Chai, Faye Chan, James P. Lodolce, David L. Boone, and Averil Ma. "Interleukin (IL)-15Rα–deficient Natural Killer Cells Survive in Normal but Not IL-15Rα–deficient Mice." Journal of Experimental Medicine 197, no. 8 (April 14, 2003): 977–84. http://dx.doi.org/10.1084/jem.20021836.

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Natural killer (NK) cells protect hosts against viral pathogens and transformed cells. IL-15 is thought to play a critical role in NK cell development, but its role in the regulation of peripheral NK cells is less well defined. We now find that adoptive transfer of normal NK cells into mice lacking the high affinity interleukin (IL)-15 receptor, IL-15Rα, surprisingly results in the abrupt loss of these cells. Moreover, IL-15Rα–deficient NK cells can differentiate successfully in radiation bone marrow chimera bearing normal cells. Finally, adoptively transferred IL-15Rα–deficient NK cells survive in normal but not IL-15Rα–deficient mice. These findings demonstrate that NK cell–independent IL-15Rα expression is critical for maintaining peripheral NK cells, while IL-15Rα expression on NK cells is not required for this function.
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Wu, Zheng, Hai-Hui Xue, Jérôme Bernard, Rong Zeng, Dmitry Issakov, Julie Bollenbacher-Reilley, Igor M. Belyakov, SangKon Oh, Jay A. Berzofsky, and Warren J. Leonard. "The IL-15 receptor α chain cytoplasmic domain is critical for normal IL-15Rα function but is not required for trans-presentation." Blood 112, no. 12 (December 1, 2008): 4411–19. http://dx.doi.org/10.1182/blood-2007-03-080697.

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AbstractIL-15 is critical for natural killer (NK)–cell development and function and for memory CD8+ T-cell homeostasis. The IL-15 receptor consists of IL-15Rα, IL-2Rβ, and the common cytokine receptor γ chain (γc). IL-15Rα is known to “trans-present” IL-15 to an IL-2Rβ/γc heterodimeric receptor on responding cells to initiate signaling. To investigate the importance of the IL-15Rα cytoplasmic domain, we generated a chimeric receptor consisting of the extracellular domain of IL-15Rα and intracellular domain of IL-2Rα (IL-15Rαext/IL-2Rαint) and examined its function in 32D cells, in knock-in (KI) mice, and in adoptive-transfer experiments. The chimeric protein exhibited decreased cell-surface expression, and KI mice exhibited diminished NK, NKT, and CD8+ T-cell development and defects in T-cell functional responses. However, 32D cells expressing the chimeric receptor had less IL-15–induced proliferation than wild-type (WT) transfectants with similar levels of IL-15Rα expression, indicating a signaling role for the IL-15Rα cytoplasmic domain beyond its effect on expression, and demonstrating that the IL-2Rα and IL-15Rα cytoplasmic domains are functionally distinct. Interestingly, adoptive-transfer experiments indicated that the chimeric IL-15Rαext/IL-2Rαint receptor still supports trans-presentation. These experiments collectively indicate that IL-15Rα can act in cis in addition to acting in trans to present IL-15 to responding cells.
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Colpitts, Sara L., Lynn Puddington, and Leo Lefrançois. "IL-15 receptor α signaling constrains the development of IL-17–producing γδ T cells." Proceedings of the National Academy of Sciences 112, no. 31 (July 20, 2015): 9692–97. http://dx.doi.org/10.1073/pnas.1420741112.

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The development and homeostasis of γδ T cells is highly dependent on distinct cytokine networks. Here we examine the role of IL-15 and its unique receptor, IL-15Rα, in the development of IL-17–producing γδ (γδ-17) T cells. Phenotypic analysis has shown that CD44high γδ-17 cells express IL-15Rα and the common gamma chain (CD132), yet lack the IL-2/15Rβ chain (CD122). Surprisingly, we found an enlarged population of γδ-17 cells in the peripheral and mesenteric lymph nodes of adult IL-15Rα KO mice, but not of IL-15 KO mice. The generation of mixed chimeras from neonatal thymocytes indicated that cell-intrinsic IL-15Rα expression was required to limit IL-17 production by γδ T cells. γδ-17 cells also were increased in the peripheral lymph nodes of transgenic knock-in mice, where the IL-15Rα intracellular signaling domain was replaced with the intracellular portion of the IL-2Rα chain (that lacks signaling capacity). Finally, an analysis of neonatal thymi revealed that the CD44lo/int precursors of γδ-17 cells, which also expressed IL-15Rα, were increased in newborn mice deficient in IL-15Rα signaling, but not in IL-15 itself. Thus, these findings demonstrate that signaling through IL-15Rα regulates the development of γδ-17 cells early in ontogeny, with long-term effects on their peripheral homeostasis in the adult.
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Schluns, Kimberly S., Kimberly D. Klonowski, and Leo Lefrançois. "Transregulation of memory CD8 T-cell proliferation by IL-15Rα+ bone marrow–derived cells." Blood 103, no. 3 (February 1, 2004): 988–94. http://dx.doi.org/10.1182/blood-2003-08-2814.

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AbstractInterleukin 15 (IL-15) and the IL-15 receptor α (IL-15Rα) chain are both required for the basal proliferation of memory CD8 T cells, but which cell types are required to express IL-15 or IL-15Rα to mediate this proliferation is not known. Using bone marrow (BM) chimeras, we showed that virus-specific CD8 memory T-cell proliferation was driven by IL-15 produced by either BM-derived or parenchymal cells. Experiments using mixed BM chimeras showed that IL-15Rα expression by memory CD8 T cells was not required for their division. In addition, wild-type memory CD8 T cells did not divide after transfer into IL-15Rα-/- mice. Further analyses demonstrated that IL-15Rα+ BM-derived cells were crucial in driving memory CD8 T-cell division in the spleen while both parenchymal and BM-derived cells promoted memory cell division in the lung. Proliferation in response to soluble IL-15 in vivo required expression of IL-15Rα by opposing cells and IL-15Rβ by CD8 memory cells, indicating that IL-15 interacted directly with the T cells. These results indicate that transpresentation of IL-15 by IL-15Rα on BM-derived cells mediates the basal proliferation of memory CD8 T cells. (Blood. 2004;103:988-994)
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Chen, Jing, Mike Petrus, Richard Bamford, Joanna H. Shih, John C. Morris, John E. Janik, and Thomas A. Waldmann. "Increased serum soluble IL-15Rα levels in T-cell large granular lymphocyte leukemia." Blood 119, no. 1 (January 5, 2012): 137–43. http://dx.doi.org/10.1182/blood-2011-04-346759.

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AbstractLarge granular lymphocyte (LGL) leukemia is a clonal lymphoproliferative disease of mature T and natural killer cells. The etiology of LGL leukemia is unknown. IL-15 is an inflammatory cytokine that stimulates T and natural killer cells and is critical for their survival and proliferation. IL-15 signals through a heterotrimeric receptor that is composed of a private receptor, IL-15Rα and IL-2/IL-15Rβ and γc shared with IL-2. Using a newly developed assay, we demonstrated increased levels of soluble IL-15Rα in the serum of patients with T-LGL leukemia. Furthermore, IL-15Rα mRNA levels were also up-regulated in the PBMCs of these patients. FACS analysis indicated that IL-15Rα was expressed both on monocytes as well as on some CD8+ leukemic cells of the patients. Interestingly, the mRNA levels of IFN-γ, a known inducer of IL-15Rα, were also up-regulated in patients' PBMCs. Moreover, PBMCs of some T-LGL patients proliferated at higher levels in response to exogenously added IL-15 compared with those of normal donors. In summary, our study demonstrated increased expression of IL-15Rα in T-LGL leukemia. It is conceivable that higher IL-15Rα expression may lower IL-15 response threshold in vivo and, therefore, may contribute to the pathogenesis of the disease.
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Dissertations / Theses on the topic "IL-15Rα"

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Desbois, Melanie. "Étude d’un nouvel agent immuno-modulateur sushi-IL-15Rα/IL-15, le RLI : évaluation de son potentiel thérapeutique dans le traitement des cancers." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T030.

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Chez les patients, la tumeur développe une immunosuppression qui compromet les capacités des effecteurs de l’immunité à réagir. Longtemps décriée, l’immunothérapie est considérée aujourd’hui comme une thérapie à part entière avec la chirurgie, la chimiothérapie et la radiothérapie. Parmi les premières immunothérapies développées dans les années 1990, l’IL-2 forte dose fut approuvée dans le traitement du mélanome et du cancer du rein métastatiques. Cependant, sa forte toxicité et la faible proportion de patients répondeurs ont limité son usage clinique. Une autre cytokine, l’IL-15, apparaît prometteuse dans le traitement des cancers pour son activité similaire à l’IL-2 sans ses facteurs limitants. Cependant, seule, son activité anti-tumorale n’est pas optimale du fait de sa courte demi-vie ou encore de l’affinité intermédiaire de liaison à son récepteur βγ. Différentes stratégies ont été mises au point pour améliorer l’efficacité de l’IL-15, notamment, sa stabilisation à travers l’association avec sa chaine de haute affinité IL-15Rα. Une molécule de fusion associant de manière covalente la partie sushi+ de l’IL-15Rα avec l’IL-15 humaine a été développée : le RLI. Au cours de cette thèse, nous avons étudié chez la souris, le potentiel thérapeutique de cette molécule dans le traitement des cancers solides. Nous avons ainsi mis en évidence une activité anti-tumorale du RLI et une association synergique avec un anticorps monoclonal anti-PD-1
In cancer patients the immune system is compromised by the tumor and its microenvironment. In recent decades the role of the immune system in tumor control has been controversial, though today cancer treatments that modulate immunity are a reality. Immunotherapy is a unique therapy adding to pre-existing methods of cancer control: surgery, chemotherapy and radiotherapy. In the 1990’s, high dosing of IL-2 was the first immunotherapy approved by the FDA to treat metastatic melanoma and renal carcinoma, however high toxicities and low responder rates have limited its clinical use. IL-15 is another promising cytokine therapy. The similar properties with IL-2 and differences in terms of toxicities and Treg induction make IL-15 an attractive potential therapy. Nonetheless, the short half-life and intermediate affinity for its receptor βγ compromise its efficacy. Different strategies have been developed to facilitate IL-15 therapeutic bioactivity. IL-15Rα as a chaperon molecule allows stability of IL-15 in vivo. RLI is a fusion molecule that covalently links sushi+IL-15Rα, the binding domain of its high affinity receptor and a recombinant human IL-15. We have studied the therapeutic potential of RLI in mouse tumor models. Our results show anti-tumor activities of RLI and synergistic combination with anti-PD-1, a monoclonal antibody
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Cepero, Donates Yuneivy. "Pathogenic role of IL-15 in non-alcoholic fatty liver disease." Mémoire, Université de Sherbrooke, 2014. http://hdl.handle.net/11143/5871.

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Abstract : Pro-inflammatory cytokines play a key role in pathogenesis of obesity and non-alcoholic fatty liver disease (NAFLD). IL-15 is a pro-inflammatory cytokine, which signals through a receptor complex composed of the IL-15 receptor (IL-15R) alpha chain, the IL-2/IL-15R beta chain and the common gamma chain. The functions of IL-15 have been extensively described in immune cells but less is known about its functions in others tissues such as the liver. The aim of this thesis is to investigate the role of IL-15 in fatty liver disease. C57BL/6 wildtype (WT) and IL-15 knockout (Il15[superscript -/-]) mice were maintained on high fat diet (HFD) or normal control diet (NCD). After 16 weeks, body weight, liver mass, fat accumulation in the liver, serum lipid levels and gene expression in the liver were evaluated. Intrahepatic lymphocytes (IHL) were also analysed. Primary hepatocytes were stimulated with IL-15 and chemokines gene expression was studied. IHLs were examined in WT, Il15[superscript -/-] and Il15ra[superscript -/-], as well as in macrophage- and hepatocyte-specific Il15ra[superscript -/-] mice. We found that IL-15 deficiency prevents weight gain and accumulation of lipids in the liver. Circulating levels of cholesterol and non-esterified fatty acids were elevated in WT mice but not in Il15[superscript -/-] mice. Hepatic expression of chemokines such as Ccl2, Ccl5 and Cxcl10 was increased in WT mice under HFD, but not in Il15[superscript -/-] mice. The livers of Il15[superscript -/-] and Il15ra[superscript -/-] mice also showed decreased expression of Tnfa and iNOS, and macrophage markers Cd68 and F4/80. Accordingly, stimulation of primary hepatocytes with IL-15 induced chemokine gene expression in WT but not in Il15ra[superscript -/-] hepatocytes. Furthermore, hepatocyte-specific ablation of IL-15Rαreduced infiltration of NK and NKT cells in the liver, suggesting that IL15Rα expression in the hepatocytes is needed for the recruitment and/or maintenance of the NK cell population in the liver. In conclusion, IL-15 promotes fat accumulation in the liver, and this is associated with increased inflammatory response in the liver. Increased availability of IL-15 in obesity may stimulate hepatocytes to secrete chemokines that promote hepatic inflammation resulting in fatty liver disease. IL-15Rα expression in hepatocytes appears to play a role in the maintenance of NK, NKT and iNKT cells. // Résumé : Les cytokines pro-inflammatoires jouent un rôle important dans la pathogenèse de l’obésité et la stéatose hépatique. L'IL-15 est une cytokine pro-inflammatoire qui est trans-présentée par l'IL-15Rα aux chaines IL-2/IL-15Rβ et γc. La fonction de l'IL-15 a été largement décrite dans les cellules immunitaires, mais ses fonctions dans d'autres tissus sont moins connues. Le but de ce mémoire est d'élucider le rôle de l'IL-15 dans la stéatose hépatique. Les souris C57BL/6 de type sauvage (WT) et Il15[indice supérieur -/-] ont été soumises à un régimehyperlipidique (HFD) ou à un régime normal. Après 16 semaines, le poids corporel, lamasse hépatique, l'accumulation de lipides dans le foie, les taux de lipides sériques et l'expression des différents gènes reliés à l’inflammation et au métabolisme dans le foie ont été évalués. Les lymphocytes intra-hépatiques (IHL) ont été également étudiés. Des hépatocytes primaires ont été stimulés avec IL-15, et l'expression génique de chimiokines a été déterminée. Les populations de IHLs ont été également caractérisées chez les souris WT, Il15[indice supérieur -/-] et Il15ra[indice supérieur -/-], ainsi que chez des souris dont la déficience dans l’expression d’IL-15Rα est ciblée aux macrophages ou aux hépatocytes. Nos résultats montrent que la déficience en IL-15 empêche l'accumulation de lipides dans le foie. Les taux de cholestérol et d’acides gras non estérifiés dans le sang étaient élevés chez les souris WT, mais pas chez les souris Il15[indice supérieur -/-]. L'expression hépatique des chimiokines Ccl2, Ccl5, Cxcl10 et des marqueurs de macrophages était augmentée chez les souris WT sous HFD, mais pas chez les souris Il15[indice supérieur -/-]. La stimulation des hépatocytes primaires avec l'IL-15 induit l'expression des gènes des chimiokines chez les hépatocytes WT, mais pas chez les Il15ra[indice supérieur -/-]. En outre, nous avons trouvé une infiltration réduite des cellules NK et NKT dans le foie des souris déficientes en Il15ra[indice supérieur -/-] dans les hépatocytes, ce qui suggère que l'expression d’IL15Rα chez les hépatocytes est nécessaire aurecrutement des cellules NK, NKT et / ou à leur maintien. En conclusion, nous proposons que l’IL-15 favorise l'accumulation de lipides dans le foie, et que ceci est associée à une réponse inflammatoire accrue. La disponibilité accrue de l'IL-15 dans l'obésité pourrait stimuler les hépatocytes à secréter des chimiokines ce qui favorise l'inflammation hépatique et conduirait à la stéatose hépatique. L’expression de l'IL-15Rα dans les hépatocytes semble jouer un rôle principal dans l’infiltration des cellules NK, NKT et iNKT dans le foie.
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3

Tamzalit, Fella. "Rôle de la coupure protéolytique du récepteur de l'Interleukine-15 dans la régulation de la trans-présentation : implication du complexe IL-15.IL-15Rα soluble en thérapie." Nantes, 2014. http://www.theses.fr/2014NANT02VS.

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L'interleukine-15 (IL-15) est une cytokine pléiotropique, impliquée dans l'homéostasie et la survie des cellules NK et T CD8+ mémoires via un mécanisme appelé trans-présentation. Dans une première partie, nous avons étudié le rôle de la coupure protéolytique de l'IL-15Rα sur la régulation de la trans-présentation de l'IL-15. Nous avons montré que le complexe IL-15. IL-15Rα exprimé à la surface des cellules présentatrices est coupé et internalisé par les cellules cibles. Ce mécanisme permet aux cellules cibles d'internaliser et stocker ces complexes pour leur propre survie et prolifération. Dans une deuxième partie, nous avons étudié le potentiel thérapeutique du RLI, un superagoniste de l'IL-15. Nous avons montré que le traitement des souris avec le RLI induit l'expansion et l'activation des cellules NK et T CD8+ mémoires. Cet effet est associé à la réduction du nombre de métastases pulmonaires. L'ensemble de ces résultats apporte une meilleure compréhension des mécanismes de régulation de l'IL-15 et montre également le potentiel thérapeutique du RLI comme adjuvant des stratégies thérapeutiques anti-tumorales
Interleukin-15 (IL-15) is a pleiotropic cytokine involved in the homeostasis and the survival of NK and memory CD8+ T cells via a mechanism called trans-presentation. In this study, we first investigated the role of IL-15R proteolytic cleavage on the regulation of IL-15 trans-presentation. We showed that the IL-15. IL-15R complex expressed at the surface of presenting cells is cleaved and internalized by responding cells. This mechanism allows responding cells to internalize and store these complexes for their own survival and proliferation. In the second part, we investigated the therapeutic potential of RLI, a fusion molecule between the sushi domain of IL-15R and IL-15. We showed that treatment with RLI induces the expansion and activation of NK and memory CD8+ T cells in vivo. This effect is correlated with a reduction of lung metastases. All these results allowed us to better understand the mechanisms regulating IL-15 and highlighted the therapeutic potential of RLI as an adjuvant in anti-tumor therapeutic strategies
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4

Yang, Shan Che, and 楊尚哲. "Impaired CD8+ TCRhi thymocytes post-selection proliferation in IL-15Rα-/- mice." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/53093156553632179052.

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碩士
長庚大學
生物醫學研究所
100
Interleukin-15 deficient (IL-15-/-) or IL-15Rα deficient (IL-15Rα-/-) mice exhibited reduction in peripheral CD8+ T cells. However, whether IL-15 or IL-15Rαis essential for thymic CD8 T cell development remains largely unknown. Intrathymic T cells express high levels of T cell receptor (TCRhi) and become mature single-positive (SP) thymocytes after they are positively selected. Some of these cells down regulate their surface CD69 prior to egress and are able to undergo intrathymic expansion. This premigrant expansion is therefore referred to as post-selection proliferation which contributes significantly to daily thymic output. In this study, I repeated experiments performed by previous students and demonstrated that the post-selection proliferation of mature CD8SP thymocytes is mediated by IL-15 transpresentation. The results showed by flow cytometry that compared with their wild type (WT) counterparts, CD8SP TCRhi thymocytes that undergo blastogenesis are reduced in IL-15Rα -/- mice. CD69-CD8SP TCRhi thymic premigrants are also reduced in IL-15Rα -/- mice. In addition, analysis by in vivo 5-bromo-2-deoxyuridine (BrdU) incorporation also demonstrated that expansion of CD8SP TCRhi thymocytes was reduced in IL-15Rα -/- mice. Based on these observations, the peripheral CD8+ T cell reduction in IL-15Rα -/- mice may be partially attributed to their defective expansion in the thymus.
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Lin, Shih Cheih, and 林士傑. "IL-15Rα-/- dendritic cells primed CD4+ T cells into hyperproliferation and IL-10 overproduction upon restimulation." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/70786057055507799376.

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碩士
長庚大學
生物醫學研究所
98
IL-15 transpresentation has been demonstrated indispensable for the development and homeostasis of CD8+ T cells, natural killer cells, and natural killer dendritic cells. Yet, its role for CD4+ T cells has never been elucidated. We here demonstrated that compared with their wild type (wt) counterparts primed in wt mice, IL-15Rα-/- CD4+ T cells primed in IL-15Rα-/- mice were hyperproliferated and produced enhanced amounts of IL-10 upon restimulation. This phenomenon also applied to alternative immunization route and antigen. Results from subsequent substitution of TCR transgenic CD4+ T cells for endogenous IL-15Rα-/- CD4+ T cells further revealed that the observed hyperproliferation and enhanced IL-10 production was independent of in vivo primed CD4+ T cells, but was attributed to the IL-15Rα-/- microenvironment. Direct in vitro stimulation of CD4+ T cells by IL-15Rα-/- dendritic cells (DCs) in the presence of cognate antigen resulted in effector cells that were hyperproliferation and overproduced IL-10 upon restimulation. Our results suggested that CD4+ T cells hyperproliferated and generated enhanced IL-10 production during restimulation when they were primed by IL-15Rα-/- DCs. These results lead us to speculate that IL-15 transpresentation plays a major role in adequate CD4+ T cell priming. In the absence of IL-15 transpresentation, CD4+ T cells differentiate into a state where the proliferation and overall IL-10 production would be enhanced upon restimulated.
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Wu, Ning Ning, and 吳甯甯. "Studies of the tolerogenic potentials of IL-15Rα-/- bone marrow-derived dendritic cells." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/56603365156764245432.

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碩士
長庚大學
生物醫學研究所
101
We have previously reported that compared to their counterparts primed in wild type (WT) mice, CD4 + T cells primed in IL-15Rα-/- mice produced more IL-10 and hyperproliferated upon in vitro restimulation. Subsequent studies revealed that IL-15Rα-/- splenic conventional dendritic cells (cDCs) are the major contributing factor to this phenomenon. In this study, we investigated whether bone marrow (BM)-derived IL-15Rα-/- DCs exhibited similar activities with their WT counterparts. We concluded that there is no difference in the phenotypes of WT and IL-15Rα-/- BM-DCs as well as their activities to prime naïve CD4+ T cells into proliferation. In contrast, compared with their counterparts primed by WT BM-DCs, OT-II CD4+ T cells primed by IL-15Rα-/- BM-DCs overproduced IL-10 upon polyclonal restimulation. However, whether IL-15Rα-/- BM-DCs-primed CD4+ T cells are restimulated to hyperproliferate requires further investigation. In addition, by neutralizing IL-15 signaling using a blocking Ab, we showed that activated WT BM-DCs overproduced IL-10 in the absence of IL-15 transpresentation, partially unveiling the skewed nature of IL-15Rα-/- BM-DCs to prime CD4+ T cells into IL-10 overproduction.
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Drasdo, Mojgan [Verfasser]. "The role of the IL-15Rα [IL-15R-alpha] cytoplasmic domain in the IL-15 signal transduction pathway / vorgelegt von Mojgan Drasdo." 2004. http://d-nb.info/971276560/34.

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Votavová, Petra. "Potenciace biologické aktivity IL-2 a IL-15 in vivo." Master's thesis, 2012. http://www.nusl.cz/ntk/nusl-310571.

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5 Abstract Interleukin-2 possesses strong stimulatory activity for activated T and NK cells and thus it is an attractive molecule for immunotherapy. However, its unfavourable pharmacological properties, extremely short half-life and severe toxicities associated with high-dose IL-2 are the most serious and limiting drawbacks. Moreover, IL-2 has been also implicated in the homeostasis of T regulatory cells where it plays a decisive role as an essential growth factor of these cells. Several different approaches to improve the therapeutic potential of IL-2 have been studied. Recently described IL-2/anti-IL-2 mAb immunocomplexes which show much higher and selective biological activity in contrast with free IL-2 in vivo are probably the most promising of them. In this study, we compared the biological activity of free IL-2 with IL-2/anti-IL-2 mAb immunocomplexes in order to demonstrate their benefits over free IL-2. We also demonstrated that IL-2/anti-IL-2 mAb immunocomplexes possess noticeable antitumor activity in two syngeneic mouse tumor models, namely EL4 T lymphoma and B16F10 melanoma, if administered early in tumor progression. Therefore, we justified potential use of IL-2/anti-IL-2 mAb immunocomplexes in tumor immunotherapy. We covalently conjugated IL-2 to synthetic semitelechelic polymeric carrier based...
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Book chapters on the topic "IL-15Rα"

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Wherry, E. John, Todd C. Becker, David Boone, Murali-Krishna Kaja, Averil Ma, and Rafi Ahmed. "Homeostatic Proliferation But not The Generation of Virus Specific Memory CD8 T Cells is Impaired in the Absence of IL-15 or IL-15Rα." In Advances in Experimental Medicine and Biology, 165–75. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0757-4_22.

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Laouar, Yasmina. "IL-15 and IL-15Rα: Something old, something new, and something blue." In Successes and Challenges of NK Immunotherapy, 143–61. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-824375-6.00007-2.

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Conference papers on the topic "IL-15Rα"

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Elpek, Kutlu G., Mark P. Rubinstein, Angelique Bellemare-Pelletier, Ananda W. Goldrath, and Shannon J. Turley. "Abstract 3829: Chronic stimulation with IL-15/IL-15Rα complexes leads to NK cell dysfunction." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3829.

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Siegler, Elizabeth L., and Pin Wang. "Abstract A59: Expression of membrane-bound IL-15/IL-15Rα complex in chimeric antigen receptor-engineered natural killer cells for enhanced efficacy against solid tumors." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a59.

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Wu, Jen-Chine, Jung-Tung Hung, Jing-Rong Huang, and Alice L. Yu. "Abstract 3506: IL-15 or IL-15/IL-15Rα complexes activates natural killer cells and enhances anti-GD2 monoclonal antibody-mediated antibody-dependent cellular cytotoxicity in vitro and in vivo." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3506.

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Desbois, Mélanie, Coralie Beal, Clelia Coutzac, Magali Terme, Geraldine Teppaz, Sebastien Morisseau, David Bechard, Erwan Mortier, and Nathalie Chaput. "Abstract 2577: RLI, a sushi-IL-15Rα/IL-15 fusion protein, is a potent immunomodulatory agent on NK and CD8+ T cells and synergizes with anti-PD1 treatment in preclinical mouse tumor models." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2577.

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Wrangle, John, Vamshidar Velchetti, Manish Patel, Samantha Suriano, Marzena Swiderska-syn, Kate Anderton, James Ravenel, et al. "Abstract B34: Safety and activity of the IL-15/sIL-15Rα complex ALT-803 in combination with the anti-PD1 mAb nivolumab in metastatic non-small cell lung cancer." In Abstracts: Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; January 8-11, 2018; San Diego, CA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.aacriaslc18-b34.

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Wrangle, John, Vamshidar Velchetti, Manish Patel, Samantha Suriano, Marzena Swiderska-syn, Kate Anderton, James Ravenel, et al. "Abstract PR05: Safety and activity of the IL-15/sIL-15Rα complex ALT-803 in combination with the anti-PD1 mAb nivolumab in metastatic non-small cell lung cancer." In Abstracts: Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic; January 8-11, 2018; San Diego, CA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.aacriaslc18-pr05.

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