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Статті в журналах з теми "Lymphoid stromal cell"
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Itoh, K., J. Friel, N. Kluge, T. Kina, A. Kondo-Takaori, S. Kawamata, T. Uchiyama, and W. Ostertag. "A novel hematopoietic multilineage clone, Myl-D-7, is stromal cell- dependent and supported by an alternative mechanism(s) independent of stem cell factor/c-kit interaction." Blood 87, no. 8 (April 15, 1996): 3218–28. http://dx.doi.org/10.1182/blood.v87.8.3218.bloodjournal8783218.
Повний текст джерелаАнотація:
A strictly stroma-dependent hematopoietic clone, Myl-D-7, with lympho- myeloid potential has been isolated. A subset of cells expresses myeloid-macrophage (Mac-1 and Gr-1), erythroid (TER119), and lymphoid (Thy-1 and B220) lineage markers. Spontaneous differentiation to the myeloid-macrophage, erythroid, or lymphoid pathway can be seen by morphologic criteria, detection of beta major globin synthesis, or expression of the early lymphoid specific transcription factor, Ikaros. By sorting lineage marker (Mac-1, Gr-1, B220, and TER119)-negative (LIN- ) cells, we showed that the LIN- population actively self-renews on top of MS-5 stromal cells, and differentiates to LIN+ cells. Removal of stroma induces apoptosis and none of the growth factors tested can prevent apoptosis. Granulocyte-macrophage colony-stimulating factor accelerates the differentiation towards the myeloid-macrophage lineage. Using this clone, we show that (1) contact with stroma induces expression of bcl-2, (2) stromal cells derived from SI/SI homozygous fetuses can support long-term growth, and (3) conditioned media of specific stromal cells contains an activity that supports proliferation and self-renewal of the clone. Myl-D-7 can thus be used as an indicator cell for unknown factors that may provide stromal cell support.
2
Kierney, PC, and K. Dorshkind. "B lymphocyte precursors and myeloid progenitors survive in diffusion chamber cultures but B cell differentiation requires close association with stromal cells." Blood 70, no. 5 (November 1, 1987): 1418–24. http://dx.doi.org/10.1182/blood.v70.5.1418.1418.
Повний текст джерелаАнотація:
Abstract The aim of this study was to investigate the relative contribution of direct contact with stromal cells v stromal cell-derived soluble mediators to the differentiation of B lymphocytes and cells from other hematopoietic lineages. This was investigated by making a comparison between hemopoietic cells grown in direct contact with stroma to those in diffusion chambers (DCs) placed over purified populations of stroma. The source of stromal cells was adherent layers from myeloid or lymphoid long-term bone marrow cultures that had been treated with mycophenolic acid, an antibiotic that depletes hemopoietic cells from the cultures but retains a functional stroma. The cells seeded into the chambers were fresh marrow cells that had been passed through two consecutive nylon wool columns to deplete cell populations capable of forming an adherent cell layer in vitro. DCs were placed in wells in which the adherent stroma, growing under myeloid or lymphoid conditions, was present. The results indicate that progenitors of granulocytes and macrophages survived and differentiated in DCs under myeloid culture conditions, as the number of cells and absolute number of CFU-GM increased over that present in the reseed population. These levels, however, were markedly less than in parallel cultures in which the cells were seeded directly onto stroma. Hematopoiesis in DCs placed over hemopoietically active stroma was not optimal, suggesting that factors were used by those hemopoietic cells closest to the stroma. A B lymphocyte precursor survived in DCs under myeloid but not lymphoid conditions, and its differentiation into B lymphocytes was dependent on close association with stromal cells; B lymphopoiesis initiated when cells from DCs grown under myeloid conditions were harvested from the chambers and seeded directly onto stroma initiated and maintained under lymphoid bone marrow culture conditions. B lymphopoiesis did not initiate if the DC from the myeloid conditions was left intact and placed directly over a lymphoid stromal cell layer in lymphoid conditions.
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Kierney, PC, and K. Dorshkind. "B lymphocyte precursors and myeloid progenitors survive in diffusion chamber cultures but B cell differentiation requires close association with stromal cells." Blood 70, no. 5 (November 1, 1987): 1418–24. http://dx.doi.org/10.1182/blood.v70.5.1418.bloodjournal7051418.
Повний текст джерелаАнотація:
The aim of this study was to investigate the relative contribution of direct contact with stromal cells v stromal cell-derived soluble mediators to the differentiation of B lymphocytes and cells from other hematopoietic lineages. This was investigated by making a comparison between hemopoietic cells grown in direct contact with stroma to those in diffusion chambers (DCs) placed over purified populations of stroma. The source of stromal cells was adherent layers from myeloid or lymphoid long-term bone marrow cultures that had been treated with mycophenolic acid, an antibiotic that depletes hemopoietic cells from the cultures but retains a functional stroma. The cells seeded into the chambers were fresh marrow cells that had been passed through two consecutive nylon wool columns to deplete cell populations capable of forming an adherent cell layer in vitro. DCs were placed in wells in which the adherent stroma, growing under myeloid or lymphoid conditions, was present. The results indicate that progenitors of granulocytes and macrophages survived and differentiated in DCs under myeloid culture conditions, as the number of cells and absolute number of CFU-GM increased over that present in the reseed population. These levels, however, were markedly less than in parallel cultures in which the cells were seeded directly onto stroma. Hematopoiesis in DCs placed over hemopoietically active stroma was not optimal, suggesting that factors were used by those hemopoietic cells closest to the stroma. A B lymphocyte precursor survived in DCs under myeloid but not lymphoid conditions, and its differentiation into B lymphocytes was dependent on close association with stromal cells; B lymphopoiesis initiated when cells from DCs grown under myeloid conditions were harvested from the chambers and seeded directly onto stroma initiated and maintained under lymphoid bone marrow culture conditions. B lymphopoiesis did not initiate if the DC from the myeloid conditions was left intact and placed directly over a lymphoid stromal cell layer in lymphoid conditions.
4
Dorshkind, K., L. Green, A. Godwin, and WH Fletcher. "Connexin-43-type gap junctions mediate communication between bone marrow stromal cells." Blood 82, no. 1 (July 1, 1993): 38–45. http://dx.doi.org/10.1182/blood.v82.1.38.bloodjournal82138.
Повний текст джерелаАнотація:
Several morphologic studies have suggested that gap junctions exist between bone marrow stromal cells. This possibility was examined by analysis of stromal cells present in the adherent layer of primary long- term lymphoid bone marrow cultures and in additional studies using a stromal cell line. Results showing that the fluorescent dye lucifer yellow, when microinjected into a single stromal cell, transferred between most other contacting stroma and that stromal cells were electronically coupled provided support that cell-cell communication occurs between these microenvironmental elements. Additional studies showed that transcripts for connexin (Cx) 43, but not for Cx26 or Cx32, were present in a stromal cell line. To examine the potential for regulated cell-cell communication between the stroma, cells were treated with interleukin-1 (IL-1), a cytokine known to affect stromal cell function, and the effects on dye transfer were examined. IL-1 treatment resulted in a reversible decrease in the ability of dye to transfer between stromal cells in contact. Taken together, these studies show that gap junctions exist between stromal cells and that their permeability can be regulated. However, gap junction-mediated cell-cell communication could not be shown between the stroma and developing lymphoid cells.
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Qotrunnada, Alvionika Nadyah, Tecky Indriana, Jane Kosasih, Meiske Margaretha, and Mei Syafriadi. "Role of cytotoxic T-lymphocyte antigen 4 (CTLA-4) expression in the pathogenesis of Warthin’s tumor growth." Dental Journal (Majalah Kedokteran Gigi) 55, no. 4 (October 12, 2022): 194–99. http://dx.doi.org/10.20473/j.djmkg.v55.i4.p194-199.
Повний текст джерелаАнотація:
Background: One of the benign salivary gland tumors is Warthin’s tumor, which is a benign tumor consisting of a papillary cystic structure covered by a double epithelial layer cells and lymphoid stroma with germinal center. Several cases have reported the Warthin’s tumor transformation into a malignant tumor such as lymphoma that develops from their stromal. Expression of cytotoxic T-lymphocyte antigen 4 (CTLA-4) as part of the immune checkpoint when highly expressed leads to a more rapid development or progression of tumors. Purpose: To analyze CTLA-4 expression in Warthin’s tumors associated with the pathogenesis of its growth through an escape mechanism from immune checkpoints and analyze based on CTLA expression whether this marker has the potential to be used as immunotherapy by administering anti CTLA-4. Methods: The tissue sections slides of Warthin’s tumor (n=8) were stained with Hematoxylin Eosin and immunostained with Recombinant Anti-CTLA4 antibody [CAL49] (ab237712). The slide with positive CTLA-4 is shown as staining on the cell membrane and/or cytoplasm. Observations were carried out using Optilab. The result is presented as figures. Results: Tumor cells expressed of CTLA-4 show in cytoplasm and/or cell membranes of the epithelial and stromal components of Warthin’s lymphoid. CTLA-4 is expressed lymphoid stroma, which is associated with inhibition of T cell activity against tumor cells, while the exact mechanism of CTLA-4 expression in epithelial components is not known but is thought to induce tumorigenesis and inhibit apoptosis. Conclusion: CTLA-4 is expressed in epithelial and stromal cells of Warthin’s tumor and this expression indicates that Warthin’s tumor cell growth is through the escape mechanism of the CTLA-4 check point immune. Further research is necessary to investigate whether CTLA-4 expression in lymphoid stroma has relate to their transformation toward a malignant tumor of lymphoma.
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Tang, J., B. L. Nuccie, I. Ritterman, J. L. Liesveld, C. N. Abboud, and D. H. Ryan. "TGF-beta down-regulates stromal IL-7 secretion and inhibits proliferation of human B cell precursors." Journal of Immunology 159, no. 1 (July 1, 1997): 117–25. http://dx.doi.org/10.4049/jimmunol.159.1.117.
Повний текст джерелаАнотація:
Abstract Development of lymphoid progenitors in vivo requires interaction with a bone marrow stromal microenvironment containing multiple cytokines involved in the development of nonlymphoid hemopoietic lineages. We tested the effect of one such cytokine, TGF-beta, on the proliferation of early human clonogenic lymphoid progenitors using a stroma-dependent in vitro culture system. TGF-beta caused a dose-dependent inhibition of lymphoid progenitor colonies that was reversible at low TGF-beta doses by addition of exogenous IL-7 to the cultures. IL-7 was unable to reverse the inhibitory effect of higher TGF-beta concentrations or inhibition caused by IL-1alpha, IL-4, or TNF-alpha. Stromal IL-7 mRNA expression and protein secretion were markedly down-regulated by TGF-beta, suggesting that inhibition of stromal IL-7 secretion partially accounts for the inhibitory effect of TGF-beta on lymphopoiesis in this culture system. It is likely that higher TGF-beta concentrations do not inhibit lymphopoiesis by down-regulating IL-7 receptor expression, since this cytokine did not reduce IL-7R alpha or gamma c mRNA levels in normal B cell precursors. Since direct stromal contact is required for in vitro lymphopoiesis, the potential regulation of the IL-7 pathway by cell adhesion was examined. Adhesion of human B cell precursors to stroma did not alter stromal IL-7 expression or expression of IL-7R alpha or gamma c-chains by B cell precursors. These results indicate that TGF-beta is a significant negative regulator of stroma-dependent proliferation of early human lymphoid progenitors and acts in part by down-regulating stromal IL-7 secretion.
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Baptista, Antonio P., and Michael Y. Gerner. "Lymphoid stromal cells proGrem dendritic cell homeostasis." Nature Immunology 22, no. 5 (April 26, 2021): 541–43. http://dx.doi.org/10.1038/s41590-021-00924-2.
Повний текст джерела
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Jankovic-Velickovic, Ljubinka, Irena Dimov, Dragan Petrovic, Slavica Stojnev, Stefan Dacic, Stefan Velickovic, and Vladisav Stefanovic. "Stromal reaction and prognosis in acinic cell carcinoma of the salivary gland." Vojnosanitetski pregled 70, no. 12 (2013): 1155–58. http://dx.doi.org/10.2298/vsp1312155j.
Повний текст джерелаАнотація:
Introduction. Primary acinic cell carcinoma (ACC) is an uncommon malignant neoplasm of the salivary gland (SG), which usually presents as slow growing tumor. Case report. We reported a 69-year-old woman with tumor in the right parotid gland with a 5-year progress. Biopsy sections revealed a hybrid form of ACC with a low- and high-grade component and prominent lymphoid tissue in tumor stroma. Immunohistochemistry was performed to define the molecular profile of this unusual ACC, with special interest for stromal influence on to the proliferative activity of ACC with dedifferentiation. We detected that the level and the type of stromal lymphoid reaction (particularly CD8+/CD4+ ratio) had a significant influence on to Ki-67 index in the high-grade component of ACC, as well as the involvement of the CXCR4 signaling axis in the stromal reaction influence. Conclusion. We suggest that tumor stroma may be a source of potential new tumor biomarkers which can determine the aggressivity of this tumor.
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Brightman, B. K., K. G. Chandy, R. H. Spencer, and H. Fan. "A T lymphoid cell line responds to a thymic stromal cell line by expression of Thy-1 and CD4." Journal of Immunology 143, no. 9 (November 1, 1989): 2775–82. http://dx.doi.org/10.4049/jimmunol.143.9.2775.
Повний текст джерелаАнотація:
Abstract We have cloned both T lymphoid and stromal lines from a single murine thymic tumor that was induced by a retrovirus carrying the v-myc oncogene (M-MuLV(myc]. The T lymphoid line, L4, was cloned by growth in agar. L4 cells were initially negative for Thy-1.2 and CD4 (although they contained rearranged TCR-beta genes), and they remained so if passaged in medium alone. However, cocultivation of these Thy-1.2- CD4- cells with the cloned stromal cell line, St3, resulted in sequential expression of Thy-1.2 and CD4 in subpopulations of cells. Thy-1.2+ CD4- and Thy-1.2+ CD4+ L4 subclones were obtained from the cocultures by subsequent cloning in agar. Derivation of these subclones from the starting Thy-1.2- CD4- clone was verified by Southern blot analyses specific for TCR-beta gene rearrangements and for M-MuLV(myc) proviral integration sites. Continuous cocultivation of Thy-1.2+ CD4+ L4 subclones with the St3 stromal cells was necessary for maintenance of CD4 on the cell surface. Furthermore, CD4 expression which was lost when CD4+ L4 cells were removed from the stroma could be reinduced if they were again cultured on St3 stroma. These cells may provide a model system for studying thymocyte-stromal cell interactions in induction and maintenance of expression of Thy-1 and CD4 molecules.
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Guilloton, Fabien, Gersende Caron, Cédric Ménard, Céline Pangault, Patricia Amé-Thomas, Joëlle Dulong, John De Vos, et al. "Mesenchymal stromal cells orchestrate follicular lymphoma cell niche through the CCL2-dependent recruitment and polarization of monocytes." Blood 119, no. 11 (March 15, 2012): 2556–67. http://dx.doi.org/10.1182/blood-2011-08-370908.
Повний текст джерелаАнотація:
Abstract Accumulating evidence indicates that infiltrating stromal cells contribute directly and indirectly to tumor growth in a wide range of cancers. In follicular lymphoma (FL), malignant B cells are found admixed with heterogeneous lymphoid-like stromal cells within invaded lymph nodes and BM. In addition, mesenchymal stromal cells (MSCs) support in vitro FL B-cell survival, in particular after their engagement toward lymphoid differentiation. We show here that BM-MSCs obtained from patients with FL (FL-MSCs) display a specific gene expression profile compared with MSCs obtained from healthy age-matched donors (HD-MSCs). This FL-MSC signature is significantly enriched for genes associated with a lymphoid-like commitment. Interestingly, CCL2 could be detected at a high level within the FL-cell niche, is up-regulated in HD-MSCs by coculture with malignant B cells, and is overexpressed by FL-MSCs, in agreement with their capacity to recruit monocytes more efficiently than HD-MSCs. Moreover, FL-MSCs and macrophages cooperate to sustain malignant B-cell growth, whereas FL-MSCs drive monocyte differentiation toward a proangiogenic and lipopolysaccharide-unresponsive phenotype close to that of tumor-associated macrophages. Altogether, these results highlight the complex role of FL stromal cells that promote direct tumor B-cell growth and orchestrate FL-cell niche, thus emerging as a potential therapeutic target in this disease.
Дисертації з теми "Lymphoid stromal cell"
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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.
Повний текст джерелаАнотація:
Les cellules stromales lymphoïdes (LSCs) sont des cellules non-hématopoïétiques essentielles à l'initiation et au maintien de réponses immunitaires performantes. Caractérisées par l'expression de la podoplanine (gp38), les LSCs sont présentes à l'état basal dans les organes lymphoïdes secondaires et sont induites par l'inflammation dans tous les tissus périphériques. Dans l'intestin, les cellules exprimant gp38 constituent la majorité des cellules non-hématopoïétiques de la lamina propria. Nous avons montré que l'expression de gp38 définit une population très hétérogène de cellules aux fonctions parfois très distinctes des LSCs. Les cellules gp38+CD34- sont des myofibroblastes sous-épithéliaux situés dns les villi et spécialisés dans la différentiation d l'épithélium. Situées dans les cryptes, les cellules gp38+CD34+VCAM+ sont similaires aux LSCs des ganglions lymphatiques : elles se développent peu après le sevrage et promeuvent l'attraction et la survie des lymphocytes. En revanche les cellules gp38+CD34+VCAM- sont programmées lors du développement embryonnaire et jouent un rôle déterminant dans le maintien de l'activité des cellules souches intestinales. Afin d'identifier les précurseurs des LSCs pendant l'inflammation, nous avons développé une souris transgénique permettant de suivre la descendance des cellules exprimant le récepteur à la lymphotoxine-beta (LTβR), une protéine essentielle au développement des ganglions lymphatiques et à la maturation des LSCs. Nous avons montré pour la première fois qu'une sous-popultion de péricytes exprimant LTβR génère des LSCs dans le ganglion pendant l'inflammationLymphoid 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
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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.
Повний текст джерелаАнотація:
Le lymphome folliculaire (FL) est le lymphome non-hodgkinien indolent le plus fréquent qui représente 20 à 25% des cas. Le FL est dans 90% des cas caractérisé par la translocation chromosomique t(14;18) des lymphocytes B, qui entraine la surexpression de BCL-2. Pour se développer, le FL est dépendant de son microenvironnement qui fournit notamment des signaux de survie et de prolifération aux lymphocytes B. Ce microenvironnement est composé en partie de cellules stromales lymphoïdes (LSC), qui, dans un contexte physiologique, structurent l’organe et soutiennent la mise en place de réactions immunitaires dans les centres germinatifs. En revanche, dans un contexte pathologique, ces cellules vont acquérir un phénotype pro-tumoral et sécréter des chimiokines telle que CXCL12, dérégulant l’homéostasie du tissus. Les mécanismes impliqués dans la transition de ces cellules vers un phénotype de type fibroblaste associé au cancer ne sont, à ce jour, pas connus. Au cours de mon projet de thèse, j’ai mis en évidence le rôle de KDM6B, une déméthylase spécifique de la marque H3K27, dans la différenciation des LSC physiologiques et pathologiques. J’ai également identifié une nouvelle voie de signalisation impliquée dans la différenciation pathologique des LSC, impliquant le facteur de transcription STAT1 sous l’influence de l’IL-4 sécrétée par les lymphocytes TFH. L’impact de l’activation de cette voie sur les lymphocytes B de FL reste encore à décrireFollicular 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
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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.
Повний текст джерелаАнотація:
Un microenvironnement riche en IL-4 a été mis en évidence dans le lymphome folliculaire (FL). Cette IL-4 impliquée dans la croissance tumorale a été démontrée comme principalement secrétée par les lymphocytes T follicular helper (Tfh). Dans cette étude, nous étudions l’interaction bidirectionnelle entre les cellules fibroblastiques réticulaires (FRC) dont le réseau est augmenté dans le FL et les lymphocytes Tfh par analyse des profils d’expression génique, et co-culture in vitro des lymphocytes Tfh primaires avec des cellules fibroblastiques humaines de type FRC-like. Nous démontrons que les cellules FRC-like augmentent in vitro la croissance des sous-populations de Tfh. De plus, nous avons mis en évidence une augmentation spécifique de la sécrétion d’IL-4 par les précurseurs Tfh (pre-Tfh) co-cultivés avec les cellules FRC-like, augmentation d’IL-4 impliquant les voies Notch et ICAM1/LFA1. Cette observation est particulièrement intéressante dans le contexte du FL car les lymphocytes pre-Tfh de FL comparés à des lymphocytes pre-Tfh d’amygdales non tumorales sont caractérisés par un profil d’expression génique enrichi en gènes des voies Notch et des intégrines en plus d’une surexpression d’IL-4. En conclusion, notre description de l’interaction entre les cellules stromales et les sous-populations Tfh démontrent une modification du profil cytokinique des Tfh au stade précurseur qui pourrait expliquer le profil cytokinique retrouvé dans le microenvironnement du FL, et apporter de nouveaux éléments pour la mise en évidence de nouvelles cibles thérapeutiquesThe 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
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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.
Повний текст джерелаАнотація:
Les polynucléaires neutrophiles ont longtemps été considérés comme des cellules n’intervenant que dans la réponse immune innée. Cependant, au cours de ces dernières années, de nombreuses publications suggèrent que ces cellules, retrouvées au sein du microenvironnement de nombreux cancers, pourraient également jouer un rôle dans la tumorigénèse et la progression tumorale. Ces études mettent en évidence leur fréquence comme marqueur pronostique dans différents cancers solides, mais peu de travaux se sont intéressés à la caractérisation fonctionnelle de ces cellules dans la progression tumorale. Dans de nombreux cancers dont les lymphomes B issus du centre germinatif, les cellules tumorales, qui sont incapables de proliférer et de survivre seules, sont dépendantes de leur microenvironnement de soutien. Dans cette étude, nous avons évalué la fonctionnalité des polynucléaires neutrophiles dans la croissance des lymphomes B. Ainsi, nous avons démontré pour la première fois que les polynucléaires neutrophiles soutiennent directement la croissance et la survie des cellules tumorales de lymphomes B. De plus, un dialogue bidirectionnel existe entre les polynucléaires neutrophiles et les cellules stromales. D’une part, les cellules stromales soutiennent la survie des polynucléaires neutrophiles, qui en retour induisent les caractéristiques d’un stroma lymphoïde. L’induction de ce phénotype permet aux cellules stromales d’acquérir de meilleures capacités de soutien envers les cellules tumorales. Cette étude confirme donc que les polynucléaires neutrophiles sont une composante importante du microenvironnement tumoral, et pourraient devenir une nouvelle cible thérapeutique pour le traitement des lymphomes B issus du centre germinatifFor 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
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Nayar, Saba. "Lymphoid like stromal cells in a model of tertiary lymphoid organ formation." Thesis, University of Birmingham, 2014. http://etheses.bham.ac.uk//id/eprint/5245/.
Повний текст джерелаАнотація:
Tertiary lymphoid organs (TLOs) are a hallmark of many chronic immune-mediated inflammatory diseases. However, till date the series of events leading to stromal cell activation in TLOs and their role in the inflammatory process remain unclear. Using a model of inducible TLO formation in the salivary glands of mice we explored the role of gp38+LTβR+ lymphoid-like stromal cells (LLSc) during TLO development and show that they acquire the capability to produce lymphoid chemokines (CKs)/cytokine and drive lymphocyte compartmentalization. In this thesis, we provide evidence that stromal cell activation is a multi-step process with three distinct phases mediated by three major cytokines (IL-13, IL-22 and LTβ). We demonstrate that during TLO formation, IL-4Rα engagement via IL-13 on quiescent tissue-resident fibroblasts induces the phenotypic acquisition of lymphoid features by LLSc. IL22 then initiates the proliferation and expansion of the LLSc population, required for the expression of lymphoid CKs/cytokines and ANA autoantibody production. Finally, we show that LTβR ligation is necessary for the establishment of a fully mature TLO structure once IL-22 driven LLSc proliferation has occurred. Based on our findings we have identified three different phases of stromal cell activation in TLOs which are all potentially targets of future therapy.
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Pandey, Shubham. "Identification of Interleukin 4 - CXCL12 supportive loop in follicular lymphoma." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B031/document.
Повний текст джерелаАнотація:
Le lymphome folliculaire (FL) est le lymphome B indolent le plus fréquent. Outre des altérations géniques récurrentes, le micro-environnement tumoral, et notamment les cellules stromales lymphoides,joue un rôle majeur dans le développement de ce cancer. Cependant, la caractérisation in-situ des cellules stromales lymphoïdes chez l'homme tout comme les facteurs menant à la polarisation du stroma en un stroma protumoral ont été peu étudiés. Dans cette thèse, nous avons montré, que les cellules stromales présentes dans les ganglions et la moelle osseuse envahis des patients atteints de FL surexpriment fortement la chimiokine CXCL12. Nous avons ensuite tenté de comprendre les mécanismes responsables de cette induction. Alors que les cellules B tumorales induisent une surexpression de la chimiokine CCL2 dans les cellules stromales de façon dépendante de leur synthèse de TNF, elles ne contribuent pas à l'induction de CXCL12. A l'inverse, le principal compartiment TCD4 impliqué dans la croissance tumorale du FL, les cellules T follicular helper (TFH), augmentent l'expression de CXCL12 dans les cellules stromales. Le taux d'IL-4, la principale cytokine produite par les TFH de FL, est d'ailleurs corrélé à celui de CXCL12 au sein de ma niche tumorale du FL. De plus, à l’aide d'un modèle de différenciation en stroma lymphoide, nous avons démontré que l’IL4 induit l’expression de CXCL12 par les cellules stromale in vitro. Cette production est augmentée quand les cellules stromales sont déjà engagées vers la voie de différentiation lymphoide par un traitement TNF/LT qui favorise l'activation de STAT6 par l'IL-4. Nous avons validé ces résultats dans un modèle de formation d'organe lymphoide ectopique chez la souris. Enfin, CXCL12 induit la migration et l'adhésion au stroma des B de FL via l'activation de cascades de signalisations qui peuvent être abrogées par l'utilisation d'un inhibiteur de Btk utilisé en clinique, l'Ibrutinib. Ces résultats sont en faveur de l'intérêt de considérer la boucle IL-4/CXCL12 pour développer de nouvelles stratégies thérapeutiques dans cette pathologie constamment fataleFollicular 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
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Lemoine, François Michel. "Studies of the interactions between stromal cells and B lymphoid progenitors." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28856.
Повний текст джерелаАнотація:
The overall goal of the work, described in this thesis was to investigate the molecular mechanisms that regulate normal pre-B cell proliferation and how these may be altered in transformed pre-B cells. Monoclonal antibodies and molecular biological techniques have allowed a number of stages of pre-B cell differentiation to be defined but little is known about mechanisms controlling their proliferation.
Studies of pre-B cell production in animal models and in long-term cultures that support pre-B cell proliferation have suggested that stromal cells play a key role in this regard. As a first step to investigate the mechanisms involved, a number of pre-B cell supportive murine stromal cell lines were isolated and characterized. A number of pre-B cell lines were also isolated, cloned and characterized. From these, spontaneous and Abelson murine leukemia virus transformants were derived. These cell lines were then used in co-culture experiments to demonstrate that stromal cells constitutively secrete a pre-B stimulating factor. Characterization of the pre-B cell stimulating activity produced by one stromal cell line (M2-10B4) showed it to be a 10 Kd molecule sensitive to freezing and different from any cloned hemopoietic growth factor described to date. The possibility that extracellular matrix components might be involved in stromal cell-mediated control of pre-B cell growth was also investigated. It was found that pre-B cells attach specifically to fibronectin and that although fibronectin by itself cannot support pre-B cell proliferation, it contributes to stromal cell stimulation of pre-B cell growth.
Both of these mechanisms were found to be affected in malignantly transformed pre-B cell populations irrespective of the mode of transformation. Transformed pre-B cells were found to have acquired the ability to secrete a novel 3 Kd autocrine factor that is also capable of stimulating normal pre-B cells. In addition transformed pre-B cells showed a greatly decreased ability to adhere to fibronectin and had become insensitive to the synergistic stimulating effect of fibronectin. It will be of interest to determine in the future whether these findings have a counterpart in human malignant pre-B cell populations.Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
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Steinthal, Nathalie Pauline Elizabeth. "Exploring the role of CD248/endosialin/TEM-1 on lymphoid stromal cells in secondary lymphoid organs." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7409/.
Повний текст джерелаАнотація:
CD248 is a pericyte-associated, mesenchymal stem cell (MSC) marker that is highly expressed during embryological life. This expression is down regulated during development, becoming restricted on lymphoid stroma to the capsule, but reappearing during inflammation, as well as in a number of disease states (Lax et al., 2007). CD248 has been shown to play a role in controlling the differentiation ofMSC to osteoblasts, both in vitro and in vivo, achieving this effect by modulating PDGFRsignalling, as treatment with the PDGFRinhibitor imatinib mesylate phenocopies the effects seen in the CD248·;. mouse (Naylor et al., 2012). Here we present evidence that CD248 is involved in the differentiation of MSC, via PDGFRsignalling, into lymphoid stroma progenitors both in vitro and in vivo. In adult mice expression of CD248 is detected on FDCs following immunisation. Using CD248·1- mice, we observe that FDC networks in CD248·1- mice do not form normally and lack the reticular, dendrite-like structure typical ofFDCs. This defect associates with a reduction in the functionality of the germinal centres. Embryonic development of lymph node stroma occurs in a stepwise manner with progressive upregulation of VCAM and ICAM on resident mesenchyme. In the adult stroma, recent work has established links between different stromal cell subtypes; Jarjour eta/. (2014) used a fate mapping technique to discover that marginal reticular cells are able to differentiate to follicular dendritic cells in response to immune challenge. Contrasting evidence shows that FDC in the spleen derive from ubiquitous perivascular precursors, likely to be pericytes (Krautler et al., 2012).
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Petitprez, Florent. "Integrated analysis and clinical impact of immune and stromal microenvironments in solid tumors Quantitative analyses of the tumor microenvironment composition and orientation in the era of precision medicine Transcriptomic analysis of the tumor microenvironment to guide prognosis and immunotherapies Tumor microenvironment quantification tool draws a comprehensive map of the tumor microenvironment of non-hematologic human cancers The mMCP-counter method to estimate abundance of tissue-infiltrating immune and stromal cell populations using gene expression in murine samples Immune sub-classes in sarcoma predict survival and immunotherapy response Intra-tumoral tertiary lymphoid structures are associated with a low risk of hepatocellular carcinoma early recurrence Association of IL-36γ with tertiary lymphoid structures and inflammatory immune infiltrates in human colorectal cancer Immune-based identification of cancer patients at high risk of progression Tumor-infiltrating and peripheral blood T-cell immunophenotypes predict early relapse in localized clear cell renal cell carcinoma PD-L1 expression and CD8+ T-cell infiltrate are associated with clinical progression in patients with node-positive prostate cancer Intratumoral classical complement pathway activation promotes cancer progression". Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB104.
Повний текст джерелаАнотація:
Les tumeurs sont composées de cellules malignes et d'une grande variété de cellules non-tumorales, en particulier des cellules immunitaires qui forment le micro-environnement tumoral (MET). Il a été démontré que la composition du MET était associée au devenir clinique des patients, en termes de survie et de réponses thérapeutiques. Avec le développement récent des immunothérapies qui ciblent des éléments spécifiques du MET, l'immunité anti-tumorale a soulevé un intérêt majeur. Plusieurs méthodologies ont été mises au point afin d'étudier la composition du MET, avec une précision toujours plus grande. En particulier, des méthodes comme MCP-counter permettent d'exploiter les données transcriptomiques de la tumeur entière afin de quantifier les différentes populations qui composent le MET. Le volet méthodologique de ce travail de thèse a ainsi consisté à proposer une amélioration de MCP-counter, en particulier pour l'analyse de données RNA-Seq. Une adaptation de la méthode pour des données issues de modèles murins (mMCP-counter) est également proposée. MCP-counter permet d'analyser rapidement le MET de larges séries de tumeurs. Un second volet de cette thèse consiste en l'application de cette méthode pour établir une classification immunitaire des sarcomes des tissus mous, un type de cancer rare, hétérogène et agressif. Cette classification immunitaire a permis de mettre en évidence des groupes de tumeurs faiblement ou fortement infiltrés, ainsi qu'un groupe marqué par une forte vascularisation. De manière intéressante, la classification immunitaire permet de prédire la réponse des patients aux immunothérapies. Ce travail a aussi démontré un rôle important des structures lymphoïdes tertiaires (SLT). Les SLT sont des structures de type noeud lymphatique composées de lymphocytes B et T qui se forment dans la tumeur ou à proximité de celle-ci. Au sein des SLT, une réponse immunitaire anti-tumorale peut se former et maturer. L'intérêt porté aux SLT est de plus en plus important pour de nombreux types de cancers. Dans la plupart des types de cancer, une forte infiltration de la tumeur par des lymphocytes T, en particulier CD8+, est associée à une meilleure survie des patients. Cependant, le carcinome rénal à cellules claires et le cancer de la prostate sont des exceptions à cette règle. En effet, dans ces deux cancers urologiques, la présence dans la tumeur de lymphocytes T est associée à une survie plus courte des patients, ainsi qu'à une rechute et une progression plus précoce. Ces exceptions sont détaillées dans une troisième partie de cette thèse, par une description minutieuse du MET, ainsi que par l'analyse de l'implication du système du complément. Dans leur ensemble, les résultats présentés dans cette thèse démontrent qu'en combinant différentes méthodes d'analyse, in silico, in situ et in vivo, il est possible d'obtenir une vision extrêmement complète du MET. La connaissance des types cellulaires présents dans la tumeur ainsi que leur orientation fonctionnelle permet de guider le soin apporté aux patients et d'améliorer leur devenir clinique. La description complète du MET ouvre la voie à une médecine personnalisée pour les patients atteints de cancerTumors are composed not only of malignant cells but also contain a vast variety of non-malignant cells, notably immune cells forming the tumor microenvironment (TME). The composition of the TME was shown to be associated with clinical outcome for cancer patients, in terms of survival and therapeutic responses. With the relatively recent development of immunotherapies targeting specific elements of the TME, tumor immunology has risen a strong interest and holds a strong therapeutic potential. Several methodologies have been developed to study the composition of the TME with an increased precision. Notably, some methods such as MCP-counter enable the use of the tumor bulk transcriptome to quantify cell populations composing the TME. The methodological aspect of this PhD project consisted in setting up an enhanced version of MCP-counter that can be readily applied to RNA-Seq data, as well as propose an adaptation of the method for mouse models. Using MCP-counter, the TME of large series of tumors can be easily analyzed. The application part of this PhD work consisted of applying MCP-counter to establish an immune-based classification of soft-tissue sarcoma, a rare, aggressive and heterogeneous cancer type. The immune classification notably allowed to identify immune low and high groups, and a group characterized by a strong vasculature. Interestingly, the classification was notably found to be predictive of the patients' response to immunotherapies. It also highlighted an important role of tertiary lymphoid structures (TLS). TLS are lymph-node-like structures composed of T and B cells that form within the tumor or in close proximity. They are a site of formation and maturation of antitumoral immune responses. TLS are raising a growing interest in many malignancies. In most cancer types, a strong infiltration by T cells, in particular CD8+ T cells, is associated with a favorable clinical outcome. However, clear-cell renal cell carcinoma and prostate cancer are exceptions to this general rule. Indeed, in these urological cancers, an increased infiltration by T cells is associated with a decreased patient survival and with earlier relapse and disease progression. In a third part of this thesis, these exceptions are investigated with more details by scrutinizing the TME, and questioning the implication of the complement system. Overall, this thesis presents how the combination of several analysis methods, in silico, in situ and in vivo, can help achieve an extremely precise description of the TME. Knowing accurately what cell populations and what their functional orientation can help guide patients care and improve clinical outcome. Complete description of the TME opens the way towards personalized medicine for cancer patients
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Dias, De Campos Joana. "The pleomorphic role of stromal cells in the formation and maintenance of tertiary lymphoid organs." Thesis, University of Birmingham, 2016. http://etheses.bham.ac.uk//id/eprint/6994/.
Повний текст джерелаАнотація:
A large body of evidence supports the role of activated stromal cells in the persistence of inflammation. The switch from resting to pathogenic stroma appears to be associated with the development of tertiary lymphoid organs (TLOs) within sites of chronic inflammation. However little is known about the immunological function of the stromal component. We utilised a murine model of inducible TLO formation in inflamed salivary glands to investigate the role of activated stromal cells characterised by the expression of gp38 and FAP during TLO development. We demonstrated that during inflammation, stroma-derived ICOSL engages ICOS on T cells, necessary for the release of lymphotoxin α and consequent TLO formation. Whilst dissecting the role of stromal cells in this context, we demonstrate that gp38 expression is required for the upregulation of adhesion molecules involved in cell clustering. Depletion of gp38+FAP+ stromal cells led to a significant reduction in lymphoid chemokine production, a decreased number of infiltrating lymphocytes and severely compromised TLO formation. Collectively, we provide evidence that activated stromal cells express FAP, provide co-stimulatory signals, and are necessary for the establishment of viral-induced TLOs, highlighting a potential novel therapeutic target in TLO-associated autoimmune diseases.
Частини книг з теми "Lymphoid stromal cell"
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Jenkinson, Eric J., Rosetta Kingston, and John J. T. Owen. "Stromal Cell Populations in the Developing Thymus of Normal and Nude Mice." In Microenvironments in the Lymphoid System, 245–49. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2463-8_30.
Повний текст джерела
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Hugo, P., R. M. Gorczynski, D. Oth, and E. F. Potworowski. "Interactions between Lymphoid Cells and a Thymic Stromal Cell Line in Vitro." In Advances in Experimental Medicine and Biology, 357–62. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5535-9_53.
Повний текст джерела
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Nadel, Helen, Barry Shulkin, Zvi Bar-Sever, and Francesco Giammarile. "Pediatric Malignancies." In A Practical Guide for Pediatric Nuclear Medicine, 199–231. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-67631-8_12.
Повний текст джерелаАнотація:
AbstractThe most common childhood malignancy is leukemia (30%), followed by brain tumors (20%), lymphomas, both Hodgkin’s (HL) and non-Hodgkin’s lymphoma (NHL) (14%), neuroblastoma (7%), soft tissue sarcoma (7%), Wilms’ tumor (6%), bone tumors (5%), germ cell tumors (3%), melanoma (3%), and hepatic tumors (1%). Their incidence varies according to patient age. Less common pediatric malignancies include head and neck cancer, Langerhans cell histiocytosis (LCH), germ cell tumors, neurofibromatosis type 1 with suspected malignant transformation, adrenocortical carcinoma, gastrointestinal stromal tumor (GIST), hepatoblastoma, hepatocellular carcinoma, carcinoid, insulinoma, and pheochromocytoma (Steliarova-Foucher et al., Lancet Oncol 18(6):719–731, 2017; Institute, NC. https://nccrexplorer.ccdi.cancer.gov/). Neuroblastoma is the second most common solid tumor in young children. It is a NET derived from the primitive neural crest. Although currently MIBG is embedded and required by international therapy protocols for patients with neuroblastoma and has a large body of evidence proving its validity and usefulness, PET tracers such as FDOPA, FDG, and 68Ga-peptides are increasingly used in imaging of neuroblastoma (Pai Panandiker et al., Clin Nucl Med 40(9):737–739, 2015). Additional pediatric NETs include ganglioneuroma, bronchial carcinoid (most common primary malignant pulmonary tumor in children), abdominal carcinoid (rare), pheochromocytoma, and PPGL. Approximately 75% of juvenile nasopharyngeal carcinomas also express surface membrane SSTRs. FDG-PET/CT is the scintigraphic study of choice for the assessment of lymphoma and sarcoma.
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Nayar, Saba, Serena Colafrancesco, and Francesca Barone. "Stromal cells in Sjögren’s syndrome." In Oxford Textbook of Sjögren's Syndrome, edited by Elizabeth J. Price and Anwar R. Tappuni, 45–50. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198806684.003.0006.
Повний текст джерелаАнотація:
The formation of tertiary lymphoid structures, defined as aggregates of lymphoid cells, developing ectopically in nonlymphoid locations, characterized by B-/T-cell segregation, differentiation of high endothelial venules, and development of follicular dendritic cells networks, supporting a germinal centre response, is a common histological feature associated with Sjögren’s syndrome. This ectopic lymphoid organization of immune cells is accompanied by the production of lymphoid chemokines and cytokines, responsible for leukocyte organization and survival. Interestingly, many of these factors detected within lymphoid structures are derived from nonhaemotopoietic stromal cells. This suggests that stromal cell activation is critically important for the maintenance and organization of tertiary lymphoid structures in inflammatory conditions.
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Schultze, Joachim L., and John G. Gribben. "B Cell Development and Maturation." In Hematopoiesis, 529–43. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780195124507.003.0047.
Повний текст джерелаАнотація:
Abstract B-lymphopoiesis is a developmentally regulated process characterized by differential phenotypic expression of a number of cell-surface and intracytoplasmic markers, immunoglobulin (lg) gene rearrangement, and, subsequently, class switching. Dysregulation of this orderly process can result in humoral deficiency, autoimmunity, or B cell malignancy (Goodnow, 1996). Increasing evidence points to the importance of interactions between the developing B cell and its microenvironment. The development of B cell-specific lineage cells is bone marrow (BM) stromal-dependent. Stromal interactions are also important in the development of antigen-specific B cells in secondary lymphoid organs, with increasing evidence pointing to the interaction of CD40 ligand with CD40 on the B cell playing an essential role here. Broadly, the process of B cell development can be divided into two stages. First, development of B cell-specific lineage cells from co34+ uncommitted progenitors. This occurs in the BM and is associated with lg recombination events. Second, development from naive to memory B cells. This is an antigen-driven process that occurs in lymphoid tissue and is characterized by acquisition of somatic hypermutation.
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Hassan Rizk, Samia. "Bone Marrow Lymphocytes' Development and Dynamics." In Lymphatic System - From Human Anatomy to Clinical Practice [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.1002915.
Повний текст джерелаАнотація:
The bone marrow (BM) is an integral part of the immune system that communicates with other immune tissues via the bloodstream but does not have lymphatic vessels. It is the primary site of lymphopoiesis, where B cells and early T-cell progenitors develop, from late fetal life onwards, and a secondary lymphoid organ for B lymphocytes. At the same time, it regulates the function and dynamics of the immune system in a steady state and disease conditions. Activating and inhibitory signals from various marrow elements regulate the traffic of lymphocyte subtypes (B, T, and NK), including direct cell contact and released factors from stromal cells. This chapter is a review of the life cycle and dynamics of lymphoid cells in health and representative immune-associated disorders. Understanding the central bone marrow’s role may clarify the pathologic changes and open potential therapeutic channels in some disorders.
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Huang, Jiawen, and Juan Huang. "Immune Checkpoint Inhibitors in Hodgkin Lymphoma and Non-Hodgkin Lymphoma." In Immune Checkpoint Inhibitors - New Insights and Recent Progress [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107435.
Повний текст джерелаАнотація:
Lymphoma, which mainly includes Hodgkin lymphoma (HL) and Non-Hodgkin lymphoma (NHL), is the most common hematological malignance of the lymphoid tissues with significantly heterogeneous characteristics. Tumor immune disequilibrium is involved in tumor development and progression, evading tumor immunosurveillance and suppressing anti-tumor immune responses. The tumor microenvironment (TME) is a complex network that comprises stromal cells and extracellular matrix, playing important roles in the pathogenesis, progression, and drug resistance of lymphoma. Therefore, a promising therapeutic strategy for lymphoma is by targeting the TME to stimulate anticancer immunity either by enhancing the release of immunostimulatory molecules or by mediating immune cell populations. Notably, immune checkpoint therapy (ICT) can provide durable clinical responses and improve overall survival in HL and NHL. However, different subsets of patients with lymphoma have different responses to ICT. Thus, significant challenges remain, including understanding pathways of resistance, optimizing patient selection, improving the management of immune-related adverse events, and identifying rational therapeutic combinations. This will allow a better understanding of the potential applications of ICT in lymphoma, guiding decisions to develop novel combination strategies with maximum efficacy and minimal toxicities for patients.
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Distler, Oliver, and Caroline Ospelt. "Rheumatoid arthritis: basic mechanisms in joints." In ESC CardioMed, 1109–12. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0271.
Повний текст джерелаАнотація:
Rheumatoid arthritis (RA) is a destructive polyarthritis which mostly starts in the small joints of the hands and feet. In the course of the disease, more proximal joints also become involved. The progressive destruction of joint structures is mediated by the chronically inflamed, hyperplasic synovial tissue, which attaches to and degrades the adjacent joint cartilage. Typical changes of the RA synovium are increased cellularity in the synovial lining and sublining layer, including vascularization, giant cell formation, and immigration of immune cells. The inflammatory cell infiltrate comprises macrophages, monocytes, dendritic cells, T cells, B cells, plasma cells, innate lymphoid cells, and mast cells. These cells together with resident stromal cells (synovial fibroblasts) form a complex network and maintain inflammatory and destructive processes via the secretion of various cytokines and chemokines. Intracellularly, cytokine-activated receptor signalling is mediated via protein kinase-dependent signalling pathways, such as mitogen-activated protein kinases and Janus kinase, which leads to the activation of transcription factors and thus changes in the transcriptional programme. Gene transcription is additionally modified by epigenetic mechanisms and post-transcriptionally by microRNA.
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Zhang, 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.
Повний текст джерелаАнотація:
Hematopoietic stem cells (HSCs) are a common origin of blood cells and the intermediate progenitor cells and precursor cells including the myeloid or lymphoid lineages, which are the footstones of short-term and long-term blood regeneration. HSCs are precisely orchestrated by the constituents in the hematopoietic microenvironment in the bone marrow niches such as stromal cells, immune cells, and cytokines. The dysfunction and genetic variations of HSCs might lead to hematopoietic abnormality, haematopoietic equilibrium and even hematologic malignancies. Meanwhile, the cellular and molecular mechanisms of HSC maintenance and differentiation according to the niche are of great importance for disease administration via hematopoietic stem cell transplantation (HSCT). In the chapter, we mainly focus on the works of literature on the definition, biological phenotypes, preclinical investigation and clinical trials of HSCs, which will collectively facilitate the clinical application of HSCT and the relative regenerative medicine for hematological diseases and immune diseases in future.
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Katakai, Tomoya. "Stromal Cells in Secondary Lymphoid Organs." In Encyclopedia of Immunobiology, 473–79. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-374279-7.07011-9.
Повний текст джерелаТези доповідей конференцій з теми "Lymphoid stromal cell"
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Lyu, Mi-Ae, Lawrence H. Cheung, John W. Marks, and Michael G. Rosenblum. "Abstract 1758: Influence of stromal microenvironment on rGel/BLyS-induced cytotoxicity in diffuse large B-cell lymphoma cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1758.
Повний текст джерела
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Park, Eugene, Jingyu Chen, Andrew Moore, Maurizio Mangolini, Joseph R. Byod, Hilde Schjerven, James C. Williamson, et al. "Abstract PO-62: Overcoming venetoclax resistance in B-cell malignancies by antagonism of stromal TGF-beta-mediated drug resistance." In Abstracts: AACR Virtual Meeting: Advances in Malignant Lymphoma; August 17-19, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2643-3249.lymphoma20-po-62.
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Lustosa, Alysson Bastos, João Paulo Holanda Soares, Iago Mateus Rocha Leite, Rilciane Maria dos Reis Ribeiro, and Olívio Feitosa Costa Neto. "SECRETORY CARCINOMA BREAST IN A YOUNG MAN." In XXIV Congresso Brasileiro de Mastologia. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s1075.
Повний текст джерелаАнотація:
Introduction: Secretory carcinoma of the breast is a rare disease, accounting for approximately 0.15% of breast cancer cases. This entity was first described in a child in 1966. However, one of the largest case series with SEER data, encompassing a total of 190 patients, showed that the median age at diagnosis was 56 years, and it can affect both sexes, being much more common in women. In this same series, 58% and 40% of patients were positive for estrogen and progesterone hormone receptors, respectively. Most cases (86.86%) were well to moderately differentiated tumors without lymph node involvement. Older patients had a worse prognosis. In general, the secretory breast carcinoma has a more indolent course with excellent prognosis. The treatment is based mainly on surgery, followed by radiation therapy. The role of chemotherapy and hormone therapy in these cases is not yet well established in the literature. Parallel to basal-like breast cancer, the indolent clinical course as well as prolonged survival seems opposite to that of common triple-negative breast cancer. In most cases of secretory breast carcinoma, reaching a 92% positivity rate, there is a fusion of the ETV6-NTRK3 genes, activating aberrant cell proliferation pathways. Studies with NTRK inhibitors are being developed and will bring this therapeutic possibility soon. Due to the rarity of secretory carcinoma of the breast, notably in men, we report the case of a young man with this neoplasm. A.S.R., 20 years old, male, from Guaraciaba do Norte (CE), white, single, telecommunications technician, reported that he noticed a painless, small, stable nodule in his left breast in 2012. He did not seek medical help at the time. In June 2021, the patient suffered trauma to her left breast during a soccer match. After this event, she noticed a considerable growth of a nodule in the left breast, which became painful to palpation. He then sought medical attention in a health center and underwent an ultrasonography of the left breast in August 2021, which detected a hypoechoic nodular image, oval, with well-defined limits, and regular contours, measuring 16.1×9.6×13.7 cm, 1.8 mm away from the skin, without vascularization inside the nodule (CATEGORY: BIRADS 3); little amount of stromal and glandular tissue were observed. A core biopsy of the nodule, performed in August 26, 2022, showed atypical epithelial proliferation. Immunohistochemistry was compatible with hypersecretory atypical epithelial proliferation. After the diagnosis of secretory carcinoma of the breast, the patient was referred to the Haroldo Juaçaba Hospital, a reference hospital in oncologic treatment in the North/Northeast of Brazil, where he underwent a slide review and immunohistochemistry, which confirmed invasive carcinoma of the secretory type of breast. Staging CT scans and bone scintigraphy were performed in September 2021. Chest CT showed a nodule with irregular contours and contrast medium concentration in the left breast, in close contact with the retropectoral musculature, measuring 19×10×12 mm, in addition to adenomegaly in the right axillary region (levels I and II), measuring up to 38×27 mm. There were no other relevant findings, with no evidence of secondary disease in the abdomen and bones. Investigation of right axillary adenomegaly with core biopsy continued and was negative for neoplasia. Histological picture and immunohistochemical profile were compatible with mixed lymphoid hyperplasia, follicular, and interfollicular. In December 28, 2022, the patient underwent a left mastectomy with sentinel lymph node biopsy, which revealed a secretory invasive carcinoma, measuring 1.9×1.5 cm, grade I, lymphovascular invasion, and negative margins, no lymph nodes were involved, nipple with compromised dermis and intraductal extension. Pathological staging: pT1c pN0 (sn-). The patient is currently on adjuvant systemic treatment (chemotherapy) with good tolerance.