Relevant bibliographies by topics / Lytic granule

Academic literature on the topic 'Lytic granule'

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Published: 22 June 2024

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Journal articles on the topic "Lytic granule":

1

HSU, HSIANG-TING, Dixita Viswanath, Emily Mace, Athanasia Christakou, Martin Wiklund, Björn Önfelt, and Jordan Orange. "Lytic granule convergence is essential for NK cells to promote targeted killing while preventing collateral damage." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 131.6. http://dx.doi.org/10.4049/jimmunol.196.supp.131.6.

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Abstract NK cell activation triggers serial events leading to lysis of diseased cells: 1) granule convergence, preformed lytic granules rapidly cluster to the microtubule-organizing center (MTOC), 2) granule/MTOC polarization to the immunological synapse, and 3) degranulation, exocytosis of lytic contents onto the target cell. Granule convergence requires LFA-1 signaling and dynein motor function. Yet, it remains elusive how lytic granule convergence contributes to NK cell cytotoxicity. Using Drosophila S2 cells, we regulate NK cell signal inputs to precisely control granule convergence and degranulation. In the absence of LFA-1 signaling, the average distance of lytic granules to the MTOC increased >1.3 fold, indicating diffuse granule localization. Using imaging flow cytometery, we determined that without LFA-1, the synaptic accumulation and degranulation of lytic granules decreased by 3.3 and 2.5 fold, respectively suggesting undirected granule release. Using an ultrasound-guided-acoustic-trap-microscopy system to enforce live single NK cell with multiple target cell contacts, we determined killing efficiency with real-time granule tracking. NK cells activated by CD16 alone without co-engaging LFA-1 showed ~40% lower targeted killing and ~30% higher non-specific killing of neighboring unlabeled “bystander” S2 cells. Finally, we used ciliobrevin D, a dynein inhibitor, to physically block granule convergence in NK cells conjugated with physiologically relevant target cells. Dynein-inhibited NK cells caused ~36% increase in bystander killing. Thus, we demonstrated that NK cells converge lytic granules to improve the efficiency of targeted lytic granule secretion and prevent collateral damage to neighboring tissue.
2

Pattu, Varsha, Mahantappa Halimani, Monika Peuschel, Elmar Krause, and Jens Rettig. "Regulation of lytic granules for normal cytotoxic T lymphocyte function (P1140)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 64.17. http://dx.doi.org/10.4049/jimmunol.190.supp.64.17.

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Abstract Cytotoxic T lymphocytes (CTLs) function to kill bacterial and viral infected target cells by releasing cytotoxic components such as perforin and granzymes that are contained within lytic granules, into the infected cell. Release occurs via the fusion of lytic granules at the contact zone between infected cell and CTL, the immunological synapse (IS). Defect in the fusion of lytic granules results in the dysfunction of CTLs, the underlying cause of the fatal disease Familial Hemophagocytic Lymphohistiocytosis (FHL). In order for fusion to occur, lytic granules must first arrive, dock and prime at the IS. Mutations within Munc 13-4, a priming factor, for lytic granules, results in FHL subtype-3. We have identified the presence of additional priming factors in CTLs. Targeted gene knockouts of these priming factors resulted in defects in lytic granule fusion at the immunological synapse. These findings demonstrate the presence of more regulatory mechanisms for the most critical event in CTLs, lytic granule fusion. Using high-resolution microscopy and evanescent wave imaging we aim to dissect the precise regulation of lytic granule fusion, which in turn would give us more insight into the regulation and function of CTLs.
3

Pattu, Varsha, Ulf Matti, Mahantappa Halimani, Lisa Weins, and Jens Rettig. "Identification of the v-SNARE required for lytic granule fusion in cytotoxic T lymphocytes (176.27)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 176.27. http://dx.doi.org/10.4049/jimmunol.188.supp.176.27.

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Abstract Cytotoxic T lymphocytes (CTLs) kill target cells by secretion of cytotoxic components such as perforin and granzymes, which are contained in lytic granules. Fusion of lytic granules occurs at the contact zone between the target cell and the CTL, the immunological synapse. Soluble NSF attachment receptor (SNARE) proteins are required for all fusion events in cells, but the SNARE proteins involved in lytic granule fusion in CTLs remain unknown. Using a targeted gene knock in strategy we identified the v-SNARE that is required for lytic granule fusion in CTLs. We first used super resolution microscopy combined with careful quantification to identify the v-SNARE that is localized exclusively to lytic granules in primary mouse CTLs. By specifically cleaving the v-SNARE with a bacterial neurotoxin and by gene knock down we show a complete loss of lytic granule fusion by two independent methods - 1) LAMP1 based degranulation assay and 2) real time imaging of exocytosis using TIRF microscopy. We therefore conclude that the v-SNARE that is localizing to the lytic granules is mediating their final fusion at the IS, thereby delivering the lethal hit needed for target cell killing.
4

Burkhardt, J. K., J. M. McIlvain, M. P. Sheetz, and Y. Argon. "Lytic granules from cytotoxic T cells exhibit kinesin-dependent motility on microtubules in vitro." Journal of Cell Science 104, no. 1 (January 1, 1993): 151–62. http://dx.doi.org/10.1242/jcs.104.1.151.

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One major mechanism of cell-mediated cytolysis is the polarized secretion of lytic granules, a process which is highly dependent on microtubules. We isolated lytic granules from murine cytotoxic T cells and tested their ability to bind to and move along microtubules in vitro. In the presence of a motor-containing supernatant, the granules bound to the microtubules and moved along them at an average maximal rate of 1 microns/second. Virtually every granule could bind to microtubules, and about half translocated within a few seconds of binding. Motility required exogenous cytosolic motors, hydrolyzable nucleotides, and an intact granule membrane. Although the motor preparation used to support granule movement contains both plus- and minus-end-directed motor proteins, granule movement was strongly biased toward microtubule plus-ends. Inactivation of cytoplasmic dynein had little effect on granule binding and movement, but immuno-depletion of kinesin from the motor preparation inhibited granule binding by 50%. These results indicate that most granule movement in this assay is mediated by kinesin. The speed and direction of granule movement in vitro are sufficient to account for the release of lytic granules in the intact T cell. This model system should be valuable for studying the interactions of secretory granules with microtubules, and for identifying the regulatory factors involved.
5

Wilton, Katelynn Marie, and Daniel D. Billadeau. "Vasodilator Stimulated Phosphoprotein (VASP)-Mediated Actin Polymerization Drives Natural Killer Cell Granule Convergence." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 170.7. http://dx.doi.org/10.4049/jimmunol.200.supp.170.7.

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Abstract Natural killer (NK) cells eliminate transformed and malignant cells through a highly orchestrated series of actin and microtubule cytoskeletal rearrangements, culminating in the secretion of preformed lytic granules. Despite the importance of actin and microtubules, the roles of many molecular cytoskeletal regulators in this process have not yet been ascertained. In this study, we investigated the role of Vasodilator Stimulated Phosphoprotein (VASP), an actin regulatory protein, in NK cell-mediated cytotoxicity. Interestingly, we found that depletion of VASP inhibits NK cell cytotoxicity and that VASP co-localizes with F-actin at the NK cell – target cell cytotoxic synapse. Surprisingly, despite their co-localization, VASP depletion did not affect either F-actin accumulation at the cytotoxic synapse or conjugate formation. Instead, we found that a minority of VASP localized and biochemically co-purified with cytolytic granules. Although VASP knockdown did not affect microtubule organizing center (MTOC) polarization, it did dramatically impact lytic granule convergence to the MTOC. Significantly, VASP depletion decreased F-actin accumulation on cytolytic granules and depolymerization of F-actin with Latrunculin A impaired lytic granule convergence. Taken together, these results demonstrate a novel requirement for VASP-mediated actin polymerization in NK cell granule convergence and cytotoxicity and highlight a role for F-actin in lytic granule convergence.
6

Liu, Dongfang, Tobias Meckel, and Eric Long. "Distinct Roles of Rab27a in Lytic Granule Movement at the Plasma Membrane and in the Cytosol (89.47)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 89.47. http://dx.doi.org/10.4049/jimmunol.184.supp.89.47.

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Abstract The small GTPase Rab27a is essential for degranulation by cytotoxic T cells and natural killer (NK) cells. To test its role in granule movement we visualized lytic granules in live, unstimulated NK cells by high-speed 3-dimensional (3D) spinning disc confocal and 2-dimensional (2D) total internal reflection fluorescence (TIRF) microscopy. Movement was tracked and quantified by automated image analysis of thousands of granules. Pharmacological inhibitors showed that long-range, directed 3D movement required microtubules (MT) but not actin, whereas 2D movement under the plasma membrane required actin dynamics. The role of Rab27a was examined by shRNA-mediated knockdown in a human NK cell line and by using NK cells from Rab27a-mutant Ashen mice. Fewer lytic granules reached the plasma membrane in the absence of Rab27a. Rab27a promoted actin-dependent, directed movement under the plasma membrane. In contrast, Rab27a reduced tracking along MT and diffusion of lytic granules in the cytosol. Therefore, Rab27a promotes delivery of lytic granules to, and movement at the plasma membrane, and has a distinct role in the cytosol, where it serves as tether to constrain lytic granule movement.
7

Peña, S. V., D. A. Hanson, B. A. Carr, T. J. Goralski, and A. M. Krensky. "Processing, subcellular localization, and function of 519 (granulysin), a human late T cell activation molecule with homology to small, lytic, granule proteins." Journal of Immunology 158, no. 6 (March 15, 1997): 2680–88. http://dx.doi.org/10.4049/jimmunol.158.6.2680.

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Abstract CTL and NK cells share a common cytolytic mechanism that involves regulated exocytosis of lytic molecules stored within cytoplasmic granules. Here we describe the processing, subcellular localization, and function of a T and NK cell-specific granule protein that shares homology with small, lytic granule-associated molecules. The gene coding for this protein, 519, is expressed late after T cell activation. Antisera raised against a 519/glutathione-S-transferase fusion protein and a series of peptides derived from the 519 protein sequence permitted the identification of two small CTL protein products of 15 and 9 kDa that are exocytosed after stimulation through the TCR. The 9-kDa product is a processed form of 519 and differs from the 15-kDa product in both its amino and carboxyl terminus. While both 519 proteins are found in cytoplasmic granules, the 9-kDa form is also present in dense, highly cytolytic granules. Functional studies indicate that this protein is lytic against tumor cell targets. The cell type- and stage-specific expression pattern of 519 along with its subcellular localization are reminiscent of molecules that play a vital role in granule-mediated cytolysis by CTL and NK cells. Its lytic activity suggests the involvement of 519 in CTL effector function.
8

Sanborn, Keri B., Gregory D. Rak, Saumya Y. Maru, Analisa Difeo, John A. Martignetti, Remi Favier, Pinaki P. Banerjee, and Jordan S. Orange. "Myosin IIA associates with NK cell lytic granules to enable their interaction with F-actin and function at the immunological synapse (134.13)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 134.13. http://dx.doi.org/10.4049/jimmunol.182.supp.134.13.

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Abstract NK cell cytotoxicity requires the formation of an actin-rich immunological synapse (IS) with a target cell and the polarization of perforin-containing lytic granules toward the IS. Following the polarization of lytic granules, they traverse through the actin-rich IS to join the NK cell membrane in order for the directed secretion of their contents to occur. We examined the role of myosin IIA in facilitating this pre-final step in lytic NK cell IS function. Lytic granules in and derived from a human NK cell line, or ex vivo human NK cells, were constitutively associated with myosin IIA. When isolated using density gradients, myosin IIA-associated NK cell lytic granules directly bound to F-actin and the interaction was sensitive to the presence of ATP under conditions of flow. In NK cells from patients with a nonsense mutation in myosin IIA, NK cell cytotoxicity, lytic granule penetration into F-actin at the IS, and interaction of isolated granules with F-actin were all decreased. Similarly, inhibition of myosin function also diminished the penetration of lytic granules into F-actin at the IS, as well as their final approach to and their dynamics at the IS. Thus, NK cell lytic granule-associated myosin IIA enables their interaction with actin and final transit through the actin-rich IS to the synaptic membrane, and can be defective in the context of naturally occurring human myosin IIA mutation. Supported by NIH grants R01 AI067946 (JSO) and T32-GM07229 (KBS).
9

Kurowska, Mathieu, Nicolas Goudin, Nadine T. Nehme, Magali Court, Jérôme Garin, Alain Fischer, Geneviève de Saint Basile, and Gaël Ménasché. "Terminal transport of lytic granules to the immune synapse is mediated by the kinesin-1/Slp3/Rab27a complex." Blood 119, no. 17 (April 26, 2012): 3879–89. http://dx.doi.org/10.1182/blood-2011-09-382556.

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Abstract Cytotoxic T lymphocytes kill target cells via the polarized secretion of cytotoxic granules at the immune synapse. The lytic granules are initially recruited around the polarized microtubule-organizing center. In a dynein-dependent transport process, the granules move along microtubules toward the microtubule-organizing center in the minus-end direction. Here, we found that a kinesin-1–dependent process is required for terminal transport and secretion of polarized lytic granule to the immune synapse. We show that synaptotagmin-like protein 3 (Slp3) is an effector of Rab27a in cytotoxic T lymphocytes and interacts with kinesin-1 through the tetratricopeptide repeat of the kinesin-1 light chain. Inhibition of the Rab27a/Slp3/kinesin-1 transport complex impairs lytic granule secretion. Our data provide further molecular insights into the key functional and regulatory mechanisms underlying the terminal transport of cytotoxic granules and the latter's secretion at the immune synapse.
10

Halimani, Mahantappa, Varsha Pattu, Christian Junker, Misty Marshall, Eva Schwarz, Elmar Krause, Ulf Matti, Markus Hoth, and Jens Rettig. "The role of syntaxin11 in cytotoxic T lymphocytes (109.26)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 109.26. http://dx.doi.org/10.4049/jimmunol.186.supp.109.26.

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Abstract Cytotoxic T Lymphocytes (CTLs) form immunological synapses (IS) with antigen presenting cells in order to kill them. Killing requires release of lytic granules which occurs via exocytosis, and is dependent on SNARE (Soluble N-ethylmaleimide sensitive factor attachment protein receptor) proteins. Syntaxin11 is a SNARE protein that is predicted to be involved in the fusion of lytic granules in CTLs, since mutations within the coding region of Syntaxin11 lead to Familial Hemophagocytic Lymphohistiocytosis (FHL4), an immune disorder caused by impaired granule exocytosis. We have investigated the contribution of Syntaxin11 to lytic granule release. We used live cell imaging to observe the trafficking of full length Syntaxin11. Using CD3 specific antibodies as a marker for a functional IS, we show that Syntaxin11 accumulates at the IS after CTL polarization and conjugation with the APC has occurred. Syntaxin11 was also associated with Munc18-2, consistent with the role of Munc18-2 as a syntaxin chaperone and as a docking factor. Using a Syntaxin11 antibody we also confirmed the subcellular localization of Syntaxin11 in fixed CTLs with confocal microscopy. Syntaxin11 was associated with Munc18-2 and CD3 at the IS in fixed CTLs, consistent with our observations in live cell imaging of CTLs. These results support the conclusion that Syntaxin11 is involved in lytic granule exocytosis.
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Journal articles

Dissertations / Theses on the topic "Lytic granule":

1

Ming, Min [Verfasser], and Jens [Akademischer Betreuer] Rettig. "Simultaneous capacitance and TIRF measurements from lytic granule fusion in primary human cytotoxic T lymphocytes / Min Ming. Betreuer: Jens Rettig." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2015. http://d-nb.info/1065232608/34.

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Tsun, Andy. "The mechanisms underlying polarised secretion of lytic granules in cytotoxic T-Lymphocytes." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510251.

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Saeed, Mezida Bedru. "Nanoscale rearrangements in cortical actin filaments at lytic immunological synapses." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/nanoscale-rearrangements-in-cortical-actin-filaments-at-lytic-immunological-synapses(8d00dd58-7b1a-435b-ad6c-016b12ff34d9).html.

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Lytic effector function of Natural Killer (NK) cells and CD8+ T cells occurs through discrete and regulated cell biological steps triggered by recognition of diseased cells. Recent studies of the NK cell synapse support the idea that dynamic nanoscale rearrangements in cortical filamentous (F)-actin are a critical cell biological checkpoint for lytic granule access to NK cell membrane. Loss of function mutations in the LYST gene, a well-characterised cause of Chediak- Hegashi syndrome (CHS), result in the formation of giant lysosomal organelles including lytic granules. Here, we report a mismatch between the extent of cortical F-actin remodelling and enlarged lytic granules that limits the functionality of LYST- deficient NK cells in a human model of CHS. Using super-resolution stimulated emission depletion (STED) microscopy we found that LYST-deficient NK cells had nanoscale rearrangements in the organisation of cortical actin filaments that were indistinguishable from control cells- despite a 2.5-fold increase in the size of polarised granules. Importantly, treatment of LYST-deficient NK cells with actin depolymerising drugs increased the formation of small secretory domains at the synapse and restored their ability to lyse target cells. These data establish that sub-synaptic F-actin is the major factor limiting the release of enlarged lytic granules from CHS NK cells, and reveal a novel target for therapeutic interventions. While the importance of cortical actin filaments in NK cell cytotoxicity have been established, its persistence at the early stages of T cell synapse formation is disputed. We studied the organisation of cortical actin filaments in synapses formed by primary human T cells using STED microscopy and detected intact cortical actin filaments in key T cell effector subsets including memory CD8+ T cells as early as 5-minutes post-activation. Quantitative analysis revealed that activation specific rearrangements in cortical actin filaments at both CD4+ and CD8+ T cell synapses serve to increase the space between filaments. Additionally, comparison of cytolytic T cells with freshly isolated and IL-2 activated primary NK cells revealed that rapid maturation of the cortical actin meshwork is a specific feature of CD8+ T cell lytic synapses. Using chemical inhibition of actin nucleators, we show that increased cortical relaxation is mediated primarily by the activity of actin related proteins (Arp) -2/3. Taken together, these data establish the critical requirement for dynamic rearrangements in cortical actin filaments at lytic synapses but underscore cell-specific differences in its regulation.
4

Delage, Laure. "Des déficiences génétiques comme modèles naturels pour l'étude de la régulation des checkpoints immunitaires et la caractérisation des réponses auto-immunes." Electronic Thesis or Diss., Université Paris Cité, 2021. http://www.theses.fr/2021UNIP5190.

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Des mutations récessives de NBEAL2 ont été décrites chez des patients atteints du syndrome des plaquettes grises (SPG). Ce syndrome se caractérise par une macro-thrombopénie, avec des plaquettes dénuées de granules-alpha, conduisant à des troubles de la coagulation, souvent associés à une splénomégalie. Ainsi, NBEAL2 a un rôle crucial dans le trafic des granules-alpha plaquettaires. En outre, notre laboratoire a montré que les patients avec un déficit en NBEAL2 peuvent présenter des caractéristiques cliniques semblables aux syndromes lymphoprolifératifs auto-immuns ; suggérant un rôle de NBEAL2 dans l'homéostasie immunitaire et la tolérance. Une cohorte internationale plus large de patients SPG a confirmé et décrit de nouvelles anomalies immunitaires chez ces patients (maladies auto-immunes, autoanticorps, lymphopénies). Si le rôle de NBEAL2 dans le trafic des granules est souvent étudié, le mécanisme exact conduisant au développement des manifestations auto-immunes chez les patients SPG reste inconnu. NBEAL2 appartient à une famille de protéines, impliquées dans le trafic vésiculaire, et possédant toutes un domaine BEACH conservé. Dans cette famille de protéines à domaine BEACH, une des protéines les plus proche de NBEAL2 est LRBA. LRBA est impliqué dans le recyclage de CTLA-4, un checkpoint immunitaire inhibiteur. CTLA-4 joue un rôle crucial dans la régulation des réponses immunitaires et la tolérance. Des mutations récessives de LRBA conduisent à des caractéristiques cliniques semblables aux déficiences partielles en CTLA-4 : auto-immunité, infiltrations lymphocytaires et lymphopénie B progressive. En condition physiologique, LRBA empêche la dégradation lysosomale de CTLA-4 et permet son recyclage à la membrane plasmatique. Par analogie avec LRBA, nous avons étudié l'importance de NBEAL2 dans le trafic intracellulaire des checkpoints immunitaires et nous avons apporté un nouveau regard sur son rôle dans les lymphocytes. NBEAL2 est ainsi une protéine d'échafaudage, se liant à LRBA, et impliquée dans le trafic de CTLA-4 ainsi que le trafic vésiculaire en général. Ces travaux apportent de nouvelles connaissances sur la régulation de CTLA-4 dans les lymphocytes T activés, une nouvelle liste de partenaires pour la protéine NBEAL2 ainsi qu'un nouveau modèle pour le trafic vésiculaire dans lequel est impliqué NBEAL2. Enfin, une meilleure compréhension des mécanismes conduisant à l'auto-immunité chez les patients atteints du syndrome des plaquettes grises pourrait conduire à un diagnostic plus précoce et un traitement adapté
Recessive NBEAL2 mutations have been reported in patients with Gray Platelet Syndrome (GPS). This syndrome is characterized by a macro-thrombocytopenia, with platelets lacking alpha-granules, leading to bleeding disorders, often associated with splenomegaly. Thus, NBEAL2 plays a crucial role in the trafficking of alpha-granules in platelets. Moreover, our lab has also described NBEAL2 deficiencies in patients presenting clinical features of the autoimmune lymphoproliferative syndrome, suggesting a role of NBEAL2 in immune homeostasis and tolerance. A broader international cohort of GPS patients has been described, revealing immune system abnormalities (autoimmune diseases, autoantibodies, lymphopenia). If the role of NBEAL2 in the traffic of granules is often investigated, the exact mechanism leading to the development of autoimmune manifestations in GPS patients remains unknown. NBEAL2 belongs to a protein family involved in vesicular trafficking, all of which possess a conserved BEACH domain. Within this BEACH-domain containing proteins family, one of the closest members to NBEAL2 is LRBA. LRBA is involved in the recycling of CTLA-4, an inhibitory immune checkpoint. CTLA-4 plays a crucial role in the regulation of immune responses and tolerance. Recessive mutations of LRBA lead to similar clinical features as partial CTLA-4 deficiency: autoimmunity, lymphocytic infiltrations, and progressive B lymphopenia. Physiologically, LRBA prevents the lysosomal degradation of CTLA-4 and allows its recycling to the membrane. By analogy with LRBA, we investigated the importance of NBEAL2 in immune checkpoints intracellular trafficking and we brought new insights on its role in lymphocytes. Thus, NBEAL2 is a scaffold protein, binding LRBA, and involved in CTLA-4 trafficking as well as in vesicular trafficking in general. This work brings new knowledge to the regulation of CTLA-4 in activated T lymphocytes, a list of new partners for NBEAL2 protein and a new model of vesicular trafficking in which NBEAL2 is involved. Finally, a better understanding of the mechanisms leading to autoimmunity in patients with gray platelets syndrome could lead to better diagnosis and treatment management
5

Halimani, Mahantappa [Verfasser], and Jens [Akademischer Betreuer] Rettig. "Syntaxin11 serves as a t-SNARE for the final fusion step of lytic granules in human cytotoxic t lymphocytes / Mahantappa Halimani. Betreuer: Jens Rettig." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2014. http://d-nb.info/105372523X/34.

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Lima, Patricia Daniele Azevedo 1984. "Dualidade funcional das células uNK de camundongos durante a gestação." [s.n.], 2012. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316901.

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Orientador: Áureo Tatsumi Yamada
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-20T04:02:31Z (GMT). No. of bitstreams: 1 Lima_PatriciaDanieleAzevedo_D.pdf: 2840118 bytes, checksum: 470a2cf0b7d63e81fd8f48aba5af44fc (MD5) Previous issue date: 2012
Resumo: Células Natural Killer uterina (uNK) produzem moléculas angiogênicas e citocinas críticas ao sucesso da gestação , assim como proteínas citolíticas relacionadas à resposta imune inata. Contudo, se as capacidades angiogênicas e citolíticas são provenientes de diferentes subpopulações de células uNK não é conhecido; da mesma forma, estes fenótipos ainda não são estabelecidos. Assim, a proposta inicial deste trabalho foi avaliar...Observação: O resumo, na íntegra, poderá ser visualizado no texto completo da tese digital
Abstract: Angiogenic and cytokine molecules produced by uterine natural killer (uNK) cells are critical for successful pregnancy. Cytolytic proteins are also express by uNK cells. However, it is unknown whether the angiogenic and cytolytic capacities are from different uNK subsets, or the same cells. Thus, we initially proposed to evaluate...Note: The complete abstract is available with the full electronic document
Doutorado
Histologia
Doutor em Biologia Celular e Estrutural
7

Pattu, Varsha [Verfasser]. "Syntaxin7 is required for lytic granule release from cytotoxic T lymphocytes / vorgelegt von Varsha Pattu." 2009. http://d-nb.info/100660121X/34.

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Battistuzzi, Susan C. "Basic fibroblast growth factor-induced proliferation in mouse embryonic fibroblasts augments their cytolysis by NK cell-derived lytic granules." 1992. http://hdl.handle.net/1993/17441.

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Qu, Bin [Verfasser]. "Vti1b-dependent interaction between lytic granules and recycling TCR compartments is required for efficient function of cytotoxic T lyphocytes / vorgelegt von Bin Qu." 2009. http://d-nb.info/1006896384/34.

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Book chapters on the topic "Lytic granule":

1

Capitani, Nagaja, Chiara Cassioli, Keerthana Ravichandran, and Cosima T. Baldari. "Exploiting the RUSH System to Study Lytic Granule Biogenesis in Cytotoxic T Lymphocytes." In The Immune Synapse, 421–36. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3135-5_27.

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AbstractThe Retention Using Selective Hooks (RUSH) system allows for the synchronized release of one or more proteins of interest from a donor endomembrane compartment, usually the endoplasmic reticulum, and the subsequent monitoring of their traffic toward acceptor compartments. Here we describe the RUSH system applied to cytotoxic T cells to characterize the biogenesis of lytic granules, using as a proof-of-concept granzyme B trafficking to this specialized compartment.
2

Müller, Sabina, Liza Filali, Marie-Pierre Puissegur, and Salvatore Valitutti. "Measuring CTL Lytic Granule Secretion and Target Cell Membrane Repair by Fluorescent Lipophilic Dye Uptake at the Lytic Synapse." In The Immune Synapse, 463–76. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3135-5_30.

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AbstractCD8+ cytotoxic T lymphocytes (CTL) play a key role in anti-tumor immune response. They are therefore at the heart of current immunotherapy protocols against cancer. Despite current strategies to potentiate CTL responses, cancer cells can resist CTL attack, thus limiting the efficacy of immunotherapies. To optimize immunotherapy, it is urgent to develop rapid assays allowing to assess CTL-cancer cell confrontation at the lytic synapse.In this chapter, we describe a flow cytometry-based method to simultaneously assess the extent of CTL activation and of tumor cell reparative membrane turnover in CTL/target cell conjugates. Such a method can be performed using a limited number of cells. It can therefore be employed in clinical settings when only a few patient-derived cells might be available.
3

Hsu, Hsiang-Ting, Alexandre F. Carisey, and Jordan S. Orange. "Measurement of Lytic Granule Convergence After Formation of an NK Cell Immunological Synapse." In The Immune Synapse, 497–515. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6881-7_31.

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Griffiths, G. M., and Y. Argon. "Structure and Biogenesis of Lytic Granules." In Pathways for Cytolysis, 39–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79414-8_3.

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Schirra, Claudia, Nadia Alawar, Ute Becherer, and Hsin-Fang Chang. "Separation of Single Core and Multicore Lytic Granules by Subcellular Fractionation and Immunoisolation." In The Immune Synapse, 159–67. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3135-5_11.

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Abstract:
AbstractSubcellular fractionation is an important tool used to separate intracellular organelles, structures or proteins. Here, we describe a stepwise protocol to isolate two types of lytic granules, multicore (MCG), and single core (SCG), from primary murine CTLs. We used cell disruption by nitrogen cavitation followed by separation of organelles via discontinuous sucrose density gradient centrifugation. Immunoisolation with a Synaptobrevin 2 antibody attached to magnetic beads was then used to harvest Synaptobrevin 2 positive granules for immunoblotting, mass spectrometry, electron, and light microscopy.
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"IL-2 Mediated Induction of Lytic Granules, Perforin, and BLT-Esterase in Potent, Granule-Free Cytolytic T Lymphocytes Indicates an Alternative Function of Lytic Granules." In Lymphocyte Activation and Differentiation, 669–72. De Gruyter, 1988. http://dx.doi.org/10.1515/9783110850253-105.

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Scharrig, Emilia, Maria L. Sanmillan, and Claudio G. Giraudo. "Analysis of immune synapses by τau-STED imaging and 3D-quantitative colocalization of lytic granule markers." In Methods in Cell Biology. Elsevier, 2023. http://dx.doi.org/10.1016/bs.mcb.2023.01.018.

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Donovan, J. P. "Thomas Love Peacock." In Literature of the Romantic Period, 269–83. Oxford University PressOxford, 1998. http://dx.doi.org/10.1093/oso/9780198711209.003.0013.

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Abstract:
Abstract Although Thomas Love Peacock (1785-1866) produced a substantial quantity of poetry in modes commonly practised by both the major and minor writers of his day-the meditative and loco-descriptive poem, personal lyric, mythological narrative, and verse satire-he is now regarded chiefly as the author of a kind of satirical prose fiction often considered to be peculiar to him and which an early reviewer described as combining the novel, the drama, and the essay In five novels with contemporary settings-Headlong Hall (1816), Melincourt (1817), Nightmare Abbey (1818), Crotchet Castle (1831), and Gryll Grange (1860-1)-as well as in the two historical romances Maid Marian (1822) and The Misfortunes of Elphin (1829), Peacock developed comic and critical perspectives on the fashions and opinions in the arts and public life which were current at various moments in his long career. He also wrote a number of trenchant essays examining the literature, as well as the literary culture and reputations, of the Romantic period. In 1820 Peacock ‘s friend Shelley described his ‘fine wit ‘ as ‘a strain too learned for a shallow age ‘, declaring his proper audience to be ‘the chosen spirits of the time ‘. It has since become a commonplace that his novels could never be widely popular, and his reputation has indeed been marked by the devoted connoisseurship, and occasionally by the sceptical mistrust, which are the usual extremes of response to writers whose afterlife has been both vigorous and persistent, though confined to a set of readers with a taste for intellectual comedy.

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