Academic literature on the topic 'Cellule stromale lymphoïde'
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Journal articles on the topic "Cellule stromale lymphoïde"
Shakhpazyan, Nikolay, Liudmila Mikhaleva, Arkady Bedzhanyan, Zarina Gioeva, Nikolay Sadykhov, Alexander Mikhalev, Dmitri Atiakshin, Igor Buchwalow, Markus Tiemann, and Alexander Orekhov. "Cellular and Molecular Mechanisms of the Tumor Stroma in Colorectal Cancer: Insights into Disease Progression and Therapeutic Targets." Biomedicines 11, no. 9 (August 23, 2023): 2361. http://dx.doi.org/10.3390/biomedicines11092361.
Full textMatsumoto, Mitsuru, Kikue Iwamasa, Paul D. Rennert, Takuji Yamada, Rika Suzuki, Akemi Matsushima, Masaru Okabe, Shigeru Fujita, and Minesuke Yokoyama. "Involvement of Distinct Cellular Compartments in the Abnormal Lymphoid Organogenesis in Lymphotoxin-α-Deficient Mice and Alymphoplasia (aly) Mice Defined by the Chimeric Analysis." Journal of Immunology 163, no. 3 (August 1, 1999): 1584–91. http://dx.doi.org/10.4049/jimmunol.163.3.1584.
Full textNitta, Takeshi. "Understanding the Thymic Microenvironment: the Cellular and Molecular Basis of T Cell Development." Central Asian Journal of Medical Sciences 2, no. 2 (November 25, 2016): 111–26. http://dx.doi.org/10.24079/cajms.2016.02.002.
Full textShadlinskaya, S. V. "Cellular composition and microanatomy of lymphoid formations of the vestibule of the vagina in postnatal ontogenesis." Sechenov Medical Journal 10, no. 1 (March 30, 2019): 57–62. http://dx.doi.org/10.47093/22187332.2019.1.57-62.
Full textCakala-Jakimowicz, Marta, Paulina Kolodziej-Wojnar, and Monika Puzianowska-Kuznicka. "Aging-Related Cellular, Structural and Functional Changes in the Lymph Nodes: A Significant Component of Immunosenescence? An Overview." Cells 10, no. 11 (November 12, 2021): 3148. http://dx.doi.org/10.3390/cells10113148.
Full textJansen, Caroline S., BaoHan Vo, Ewelina Sobierajska, Rachel Greenwald, Patrick Mullane, Nataliya Prokhnevska, Maria Cardenas, et al. "Abstract B030: Form and function in intratumoral immune organization: Understanding the cellular composition of TCF1+ CD8+ T cell niches in human cancer." Cancer Research 83, no. 16_Supplement (August 15, 2023): B030. http://dx.doi.org/10.1158/1538-7445.kidney23-b030.
Full textVoermans, Carlijn, and Mette D. Hazenberg. "Cellular therapies for graft-versus-host disease: a tale of tissue repair and tolerance." Blood 136, no. 4 (July 23, 2020): 410–17. http://dx.doi.org/10.1182/blood.2019000951.
Full textBaron, Chloé S., Serine Avagyan, Song Yang, Aaron McKenna, and Leonard Zon. "Abstract A27: Cellular barcoding of the leukemic niche reveals an apelin-mediated clonal expansion of niche endothelial and mesenchymal stromal cell clones." Blood Cancer Discovery 4, no. 3_Supplement (May 1, 2023): A27. http://dx.doi.org/10.1158/2643-3249.aml23-a27.
Full textAggarwal, Vaishali, Radhika Srinivasan, Amanjit Bal, Pankaj Malhotra, Gaurav Prakash, Subhash Varma, and Ashim Das. "Mutational Spectrum of Stromal Genes By Whole Exome Sequencing and Stromal-Cellular Interaction in Diffuse Large B-Cell Lymphoma." Blood 126, no. 23 (December 3, 2015): 2649. http://dx.doi.org/10.1182/blood.v126.23.2649.2649.
Full textBelli, Carmen, Gabriele Antonarelli, Matteo Repetto, Luca Boscolo Bielo, Edoardo Crimini, and Giuseppe Curigliano. "Targeting Cellular Components of the Tumor Microenvironment in Solid Malignancies." Cancers 14, no. 17 (September 1, 2022): 4278. http://dx.doi.org/10.3390/cancers14174278.
Full textDissertations / Theses on the topic "Cellule stromale lymphoïde"
Barbier, Nicolas. "Étude du rôle des mécanismes épigénétiques dans la transition des cellules stromales mésenchymateuses en fibroblastes associés au cancer et dans l’acquisition de leurs propriétés pro-tumorales dans le lymphome folliculaire." Electronic Thesis or Diss., Université de Rennes (2023-....), 2024. http://www.theses.fr/2024URENB011.
Full textFollicular lymphoma (FL) is the most common indolent non-Hodgkin's lymphoma, accounting for 20-25% of cases. In 90% of cases, FL is characterized by the chromosomal translocation t(14;18) in B lymphocytes, causing BCL-2 overexpression. FL is dependent on its microenvironment, which supplies survival and proliferation signals to the B cells. This microenvironment includes lymphoid stromal cells (LSC), which, in a physiological context, structure the organ and support the development of immune reactions in the germinal centers. However, in a pathological context, these cells acquire a protumoral phenotype and secrete chemokines such as CXCL12, deregulating tissue homeostasis. The exact process through which these cells transform into cancer- associated fibroblasts isn't fully understood. My project has therefore highlighted the role of KDM6B, a specific déméthylase of H3K27, in the differentiation of physiological and pathological LSCs. I also identified a new signaling pathway involved in LSCs pathological differentiation, involving the transcription factor STAT1, under the influence of IL-4 secreted by TFH. It remains to be described how activation of this pathway affects FL B cells
Misiak, Jan. "The interactions of stromal cells and follicular helper T cells resulting in a B-cell supporting, IL4-producing phenotype in the context of follicular lymphoma." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B030.
Full textThe enrichment of the microenvironment with tumor-promoting interleukin 4 (IL4) has been implicated in the pathogenesis of follicular lymphoma (FL) and was found to be conferred mainly by T follicular helper (Tfh) cells. In this study, we investigated the bidirectional crosstalk of fibroblastic reticular cells that are expanded in FL and Tfh cells with the analysis of gene expression profiles of the respective, and an in-vitro co-culture model of human induced FRC-like cells. We demonstrated that FRC-like cells enhance the growth of Tfh cell subsets in vitro. Crucially, we uncovered a specific upregulation of IL-4 secretion by precursor Tfh (pre-Tfh) cells co-cultured with FRC-like cells. Additionally, we demonstrated that Notch and ICAM1/LFA1 are two pathways involved in IL-4 secretion following FRClike cell / Tfh cell crosstalk. This observation was particularly interesting in FL context, because FL pre-Tfh cells display an enriched Notch and integrin gene expression profile as well as an overexpression of IL-4, compared to their tonsil counterpart. Altogether, we described new interactions between stromal cells and Tfh subsets and uncovered a specific cytokine profile modification at pre-Tfh stage after contact with FRC-like cells that could explain the high levels of IL-4 in FL and provide a novel target for therapy
Pandey, Shubham. "Identification of Interleukin 4 - CXCL12 supportive loop in follicular lymphoma." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B031/document.
Full textFollicular lymphoma (FL) is the most frequent indolent B-cell lymphoma. Beside recurrent genetic alterations, tumor microenvironment, including lymphoid stromal cells, has been shown to play a key role in FL development. However, in situ characterization of lymphoid stromal cells is still lacking in humans and there are very few studies focusing on the factors that could lead to stroma polarization in normal and pathological context. In this thesis, we showed first that in FL, lymph node (LN) and bone marrow (BM) infiltrating stromal cells highly express the chemokine CXCL12. We next focused on the mechanisms underlying this upregulation. Interestingly, whereas malignant FL B cells induced overexpression of CCL2 in stromal cells in a TNF-dependent manner, they did not contribute to CXCL12 induction. Conversely, FL-infiltrating follicular helper T cells (FL-TFH), the key FL-supportive T-cell subset could trigger CXCL12 expression in stromal cells. IL-4 is the main FL-TFH-derived cytokine and showed a positive correlation with CXCL12 expression inside FL cell niches. Moreover, based on our in vitro lymphoid stroma differentiation model, we demonstrated that IL-4 promoted CXCL12 expression in stromal cells, together with a phenotype close to that identified in situ within FL cell niche. Such IL4 dependent CXCL12 regulation is more pronounced in stromal cells already committed towards lymphoid stromal cells by a prestimulation by TNF/LT in association with an increased STAT6 activation. These data were validated in a model of ectopic lymphoid organ formation in mice. Finally, CXCL12 induced FL B-cell migration, and adhesion to stromal cells through the activation of a signaling pathway that could be abrogated by the Btk inhibitor Ibrutinib. These data argue for considering IL-4/CXCL12 axis as a potential therapeutic target to disrupt FL protective cell niche in this still fatal malignancy
Grégoire, Murielle. "Polynucléaires neutrophiles, cellules stromales, lymphocytes B : interaction tripartite dans la niche des lymphomes B." Thesis, Rennes 1, 2014. http://www.theses.fr/2014REN1S156/document.
Full textFor long time, neutrophils have only been considered as cells involved in the innate immune response. More recently, in descriptive publications, neutrophils were found in the microenvironment of many solid cancers, hypothesizing that they could also play a role in tumorigenesis and cancer progression. These studies highlighted the prognostic value of their frequency, but few of them focused on the functional characterization of these cells in tumor growth. In many cancers, including germinal centre-derived B-cell lymphomas, tumor cells are dependent on their microenvironment to proliferate and survive. In this study, we focused on the role of neutrophils in the progression of B-cell lymphomas, and for the first time we demonstrated that neutrophils directly support the growth and survival of tumor Bcells. In addition, we highlighted the existence of bidirectional cooperation between neutrophils and stromal cells. In one hand stromal cells support the survival of neutrophils. On the other hand, neutrophils induce a lymphoid stroma phenotype which is well known to enhance their supportive effect on tumor cells. This study demonstrates that neutrophils are a significant component of the tumor microenvironment and may be considered as a potential therapeutic target for the treatment of B-cell lymphomas
Lemoine, François. "Etudes des interactions entre les cellules stromales et les progeniteurs lymphoides b." Paris 7, 1989. http://www.theses.fr/1989PA077206.
Full textBresler, Priscillia. "Étude de la régulation des cellules lymphoïdes innées par les lymphocytes T chez la souris." Electronic Thesis or Diss., Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB078.
Full textMany articles in the literature report that the composition, the frequency and the activity of ILCs are strongly affected when the adaptive immune system is deficient in mice. However, the mechanisms by which adaptive immunity regulates the homeostasis of ILCs remain largely unknown. The objective of my thesis was to address the role played by T cells in this regulation within lymphoid tissues such as peripheral and mesenteric lymph nodes and in the small intestine. I also characterised some of the regulatory mechanisms involved in this dialogue between ILCs and T cells and determined their tissue specificity. During my thesis, I confirmed that the regulation of gut resident ILC3 by CD4+ T cells is based on their ability to participate in the containment and diversification of bacterial communities colonizing the gut. In addition, I have also highlighted the role of CD4+ T cells in the regulation of the frequency and activity of type 2 ILCs in the mesenteric lymph nodes. The latter does not rely on the activation of CD4+ T cells by the gut microbiota. Indeed, I showed that the expression of the gene encoding IL-33 is increased in the mesenteric lymph nodes of T cell deficient mice and that the short-term neutralization of IL-33 signalling in vivo significantly reduces the frequency of type 2 ILCs in the mLNs of these mice. In collaboration with Lucie Peduto's team, we showed that T lymphocytes indirectly regulate the expression of IL-33 by mesenteric lymph nodes stromal cells. However, the mechanisms underlying these interactions remain to be elucidated. Finally, the role of other T-cell dependent environmental factors remains to be characterised. Indeed, our preliminary results indicate that T-B cooperation may be instrumental in the regulation of mesenteric lymph nodes resident ILC2 while it is redundant in the regulation of gut resident type 3 ILCs by CD4+ T cells
Crompot, Emerence. "Caractérisation phénotypique et impact fonctionnel des vésicules extracellulaires issues de cellules stromales mésenchymateuses sur les lymphocytes B de Leucémie Lymphoïde Chronique." Doctoral thesis, Universite Libre de Bruxelles, 2017. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/245872.
Full textDoctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
Camara, Abdouramane. "Control of lymphoid organ CD169+ macrophage differentiation by stromal cells through the RANK-RANKL axis." Thesis, Strasbourg, 2019. http://www.theses.fr/2019STRAJ102.
Full textLymph node CD169 + sinusoidal macrophages are sentinel cells that recognize the danger signals and initiate the protective immune responses. However, the signals and the mechanism underlying their formation are not well known. During my thesis, I have shown that the cytokine Receptor Activator of NF-kB Ligand (RANKL) is required for their differentiation, starting from the embryogenesis up to four weeks after birth. The lymphatic endothelial cells (LECs) activated by RANKL expressed by mesenchymal cells form the niches for the primary differentiation of these macrophages. Yet, in adults, RANKL-activated LECs are required for their niche replenishment after transient depletion induced by an inflammatory stimulus. Beyond lymph node, my research has revealed a general requirement of the double signal RANKL & lymphotoxin LTα1β2 for the differentiation of non-osteoclastic CD169 + macrophages of spleen and bone marrow
Stzepourginski, Igor. "Identification of lymph node and intestinal lymphoid stromal cell subsets with key roles in immunity and homeostasis." Paris 7, 2014. http://www.theses.fr/2014PA077148.
Full textLymphoid stromal cells (LSCs) are non-hemaopoietic cells pivotal in building and maintaining efficient immune responses. LSCs are described as podoplanin (gp38)- expressing cells and are present in secondary lymphoid organs at steady state. Moreover, LSCs are induced by inflammation and some tumors in the periphery. In the intestinal lamina propria, gp38+LSCs compose the majority of the non-hematopoietic cells at steady state. We showed that gp38+intestinal stromal cells are very heterogeneous and contain cells distinct from LSCs that populate different niches in the lamina propria. Gp38+CD34- stromal cells are subepithelial myofibroblasts located in the upper lamina propria that promote the differentiation of epithelial cells. In the crypts, gp38+CD34+VCAM+ stromal cells are the equivalent of LSCs found in lymphoid organs : they develop around weaning to attract lymphocytes into the lamina propria and promote their survival. However, gp38+CD34+VCAM- stromal cells develop during ontogeny and maintain the activity of intestinal epithelial stem cells in the crypts. In order to identify LSC progenitors during inflammation we developed a transgenic mouse model allowing for the fate-mapping of cells expressing lymphotoxin beta receptor (LTβR), a key protein involved in the development of lymphoid organs and LSC maturation. We showed for the first time that a subset of pericytes expressing LTβR give rise to LSCs during inflammation-induced expansion of the lymph node
Passaro, Diana. "Dissection of phenotypic traits and molecular mechanisms underlying Cn/NFAT pathway activation in T-ALL." Paris 7, 2013. http://www.theses.fr/2013PA077263.
Full textDespite their initial efficient response to induction chemotherapy, relapse remains frequent in patients with T-ALL. Previous results from the laboratory revealed that Cn is active and has a pro-oncogenic fonction in mouse models of human T-ALL. Using an ICN1-induced T-ALL mouse model, in which conditional Cn genetic deletion is restricted to leukemic cells, we demonstrated that Cn is intrinsically required for the ability of leukemic cells to propagate the disease (LIC activity). Importantly, combination of vincristine treatment with Cn inactivation cooperated to induce long-term remission of ICN1-induced T-ALL. Phenotypically, Cn deletion altered the functional interactions between leukemic cells and the supportive MS5 stromal cell line ex vivo, resulting in reduced leukemic cell survival, proliferation, migration and clonogenic potential. At the molecular level, transcriptomic analysis revealed that Cn deletion was associated with the deregulation of the expression of >400 genes. We analysed the consequences of Cdkn la (p21) up-regulation upon Cn deletion, showing that it likely participates to the cell cycle arrest observed in Cn-deficient leukemic cells. We also found that expression of Cxcr4 was down-regulated at the surface of leukemic cells upon Cn deletion, a mechanism that we found responsible of the decreased motility of Cn-deficient leukemic cells. Finally, using ICN1- induced T-ALL mouse m odel in which NFATc 1, NFATc2 and NFATc3 genes could be conditionally inactivated, we demonstrated a role for NFAT in the survival, proliferation, motility and LIC activity of leukemic cells
Book chapters on the topic "Cellule stromale lymphoïde"
Mueller, C. G., S. Nayar, J. Campos, and F. Barone. "Molecular and Cellular Requirements for the Assembly of Tertiary Lymphoid Structures." In Stromal Immunology, 55–72. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78127-3_4.
Full textZhang, Leisheng, Xiaorong Bai, Shan Huang, Jiechao Ma, Yuan Meng, Xiaoming Feng, Tiankang Guo, and Hui Cai. "Hematopoietic Stem Cells in Regenerative Medicine." In Stem Cells in Clinical Application and Productization, 29–57. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815196627124010006.
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