Готові списки джерел за темами / Lymphocyte precursors

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Добірка наукової літератури з теми "Lymphocyte precursors"

Автор: Grafiati
Опубліковано: 11 березня 2023

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Статті в журналах з теми "Lymphocyte precursors"

1

Zhuk, Ye A., and V. A. Galenok. "T-lymphocyte precursors in diabetics." Problems of Endocrinology 41, no. 2 (April 15, 1995): 4–6. http://dx.doi.org/10.14341/probl11356.

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Patients with types I, II, and pancreatogenic diabetes mellitus were examined for the counts of T precursor cells using autorosette formation test in the presence of t-activin, an activator of T lymphocyte differentiation. The counts of T lymphocyte precursors in patients with type II and pancreatogenic diabetes were virtually the same as in normal subjects. Disorders of cellular immunity in type I diabetes mellitus were found to be associated with depletion of pre-T-lymphocytes. These changes were the most manifest in the decompensation phase (ketoacidosis state). The results may be useful in development of immunomodulating therapy for type I diabetes and in prediction of the disease development in subjects predisposed to it.
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2

Thiele, D. L., and P. E. Lipsky. "Leu-Leu-OMe sensitivity of human activated killer cells: delineation of a distinct class of cytotoxic T lymphocytes capable of lysing tumor targets." Journal of Immunology 137, no. 4 (August 15, 1986): 1399–406. http://dx.doi.org/10.4049/jimmunol.137.4.1399.

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Abstract Sensitivity to L-leucyl-L-leucine methyl ester (Leu-Leu-OMe) was used to characterize the phenotype of human activated killer cells. Natural killer cells (NK) and the precursors of both the alloantigen-specific cytotoxic T lymphocytes (CTL) and the NK-like activated killer cells generated after stimulation with allogeneic cells were deleted from human peripheral blood lymphocytes by preincubation with Leu-Leu-OMe. It was noted, however, that cytotoxic lymphocytes could be generated from Leu-Leu-OMe-treated lymphocyte precursors after 2 to 6 days of culture with the nonspecific mitogen, phytohemagglutinin (PHA). The characteristics of these killer cells indicated that they were a unique population that could be distinguished from other cytotoxic cells. Killing by these cells exhibited slow kinetics in that 18 hr cytotoxicity assays were required to detect full cytotoxic potential. When 18 hr assays were used, PHA-stimulated cytotoxic cells generated from Leu-Leu-OMe-treated lymphocytes were able to kill both NK-sensitive K562 cells and the relatively NK-resistant renal cell carcinoma cell line, Cur. These cytotoxic lymphocytes were HNK-1, Leu-11b (CD16), and OKM1 (CR3)-negative at both the precursor and effector stage of activation. Furthermore, these cells were derived from a CD3-positive precursor. Finally, killing by activated effectors was inhibited by OKT3. Unlike activation of Leu-Leu-OMe-sensitive large granular lymphocytes, generation of these cytotoxic T cells was totally prevented by treatment with mitomycin c before stimulation. Thus, a unique class of tumoricidal T cells can be characterized by resistance of lymphocyte precursors to a concentration of Leu-Leu-OMe, which has been shown to ablate NK, mixed lymphocyte culture-activated NK-like cytotoxic precursors, and the precursors of alloantigen-specific CTL.
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3

Peddie, Clare M., and Valerie J. Smith. "‘Lymphocyte-like’cells in ascidians: Precursors for vertebrate lymphocytes?" Fish & Shellfish Immunology 5, no. 8 (November 1995): 613–29. http://dx.doi.org/10.1016/s1050-4648(95)80045-x.

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4

Sanders, V. M., and F. E. Powell-Oliver. "Beta 2-adrenoceptor stimulation increases the number of antigen-specific precursor B lymphocytes that differentiate into IgM-secreting cells without affecting burst size." Journal of Immunology 148, no. 6 (March 15, 1992): 1822–28. http://dx.doi.org/10.4049/jimmunol.148.6.1822.

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Abstract Previous studies have shown that early addition of a beta 2-adrenergic agonist to whole splenocyte cultures immunized with SRBC induced an increase in the number of cells secreting Ag-specific antibody. Because of the low frequency of Ag-specific B lymphocytes in these cultures, it has been difficult to determine the cellular mechanism by which this increase is produced. To gain insight into this cellular mechanism, the present study was designed to evaluate the responsiveness of TNP-specific B lymphocytes cultured at both high density and limiting dilution with keyhole limpet hemocyanin (KLH)-specific, IL-4-producing Th lymphocytes, TNP-KLH, and the beta 2-adrenergic agonist, terbutaline. The results showed that a maximal twofold increase in both the number of anti-TNP IgM-secreting cells and the amount of anti-TNP IgM secretion occurred in terbutaline-exposed lymphocytes after 5 days of bulk culture. This response occurred in a concentration-dependent manner and was inhibited by concomitant culture with beta-adrenoceptor antagonists. No appreciable change was measured in the level of either IgG1 secretion in terbutaline plus Ag-exposed bulk cultures or MHC class II expression on terbutaline plus Ag-exposed TNP-specific B lymphocytes as compared with Ag alone. These data raised the possibility that beta 2-adrenoceptor stimulation induced either the differentiation of a larger proportion of TNP-specific B lymphocyte precursors into anti-TNP IgM-secreting cells, or the extensive proliferation of a constant number of TNP-specific B lymphocyte precursors, or both. Limiting dilution results showed that beta 2-adrenoceptor stimulation induced a twofold increase in the number of TNP-specific B lymphocyte precursors that differentiated into anti-TNP IgM-secreting cells, without affecting the number of anti-TNP IgM-secreting cells produced by each precursor clone.
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5

Griffiths, S. D., D. T. Goodhead, S. J. Marsden, E. G. Wright, S. Krajewski, J. C. Reed, S. J. Korsmeyer, and M. Greaves. "Interleukin 7-dependent B lymphocyte precursor cells are ultrasensitive to apoptosis." Journal of Experimental Medicine 179, no. 6 (June 1, 1994): 1789–97. http://dx.doi.org/10.1084/jem.179.6.1789.

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Анотація:
We have compared the sensitivity of clonogenic interleukin 7 (IL-7)-dependent murine B cell precursors with that of clonogenic mature B cells and myeloid precursors to alpha-particles from plutonium-238 and X radiation. All three populations are relatively sensitive, but B cell precursors are ultrasensitive. This differential sensitivity is also observed with corticosteroid, etoposide, and cisplatin, all apoptosis-inducing drugs used in the treatment of leukemia and other cancers. Further, we show that x-rays and drugs induce the bulk of the B cell precursor population to undergo rapid apoptosis, despite the continued presence of IL-7. B cell precursors were found to express very low levels of BCL-2 protein compared with mature splenic B cells and their resistance to x-rays and corticosteroid could be enhanced by expression of a BCL-2 transgene. These data have important implications for normal lymphopoiesis and for the behavior of leukemic lymphoid precursor cells.
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6

Skinner, M. A., R. W. Finberg, and H. C. J. Ertl. "Regulation of cytotoxic lymphocyte precursors." Cellular Immunology 100, no. 1 (June 1986): 239–46. http://dx.doi.org/10.1016/0008-8749(86)90023-7.

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7

Arvin, A. M., M. Sharp, S. Smith, C. M. Koropchak, P. S. Diaz, P. Kinchington, W. Ruyechan, and J. Hay. "Equivalent recognition of a varicella-zoster virus immediate early protein (IE62) and glycoprotein I by cytotoxic T lymphocytes of either CD4+ or CD8+ phenotype." Journal of Immunology 146, no. 1 (January 1, 1991): 257–64. http://dx.doi.org/10.4049/jimmunol.146.1.257.

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Abstract Immunity to varicella-zoster virus (VZV), a member of the alpha-herpes virus family, exemplifies the host response to an ubiquitous human viral pathogen. In this investigation of the cytotoxic T lymphocyte (CTL) response to VZV, the depletion of CD4+ T lymphocytes made it possible to demonstrate CD8(+)-mediated cytotoxic function against autologous VZV-infected lymphoblastoid cells targets. CTL recognition of two major VZV proteins, the immediate early protein (IE62) and gp I, was demonstrated in limiting dilution cultures of T lymphocytes obtained from immune donors, stimulated with inactivated VZV Ag, and tested against lymphoblastoid cells infected with vaccinia recombinants expressing these VZV proteins. Among 11 VZV donors tested at least 20 y after primary infection, the mean precursor frequency for T lymphocytes that recognized the IE62 protein was 1:105,000 +/- 85,000 SD, with a range of 1:13,000 to 1:231,000. The mean frequency of CTL precursors specific for gp I in 11 subjects was equivalent, with a mean of 1:121,000 +/- 86,000 SD (range 1:15,000 to 1:228,000) (p = 0.68). Limiting dilution cultures were also prepared using purified CD4+ or CD8+ T lymphocyte populations recovered from PBMC by sterile fluorescence-activated cell sorting. CTL precursors that recognized the IE62 protein or gp I were derived from each of the major T lymphocyte populations by stimulation with inactivated VZV Ag; CD4+ and CD8+ CTL precursor frequencies for the IE62 protein and gp I were equivalent (p = 0.2). We conclude that antiviral CTL activity against targets expressing VZV proteins was mediated equally well by T lymphocytes of the CD4+ or CD8+ phenotype and that antiviral CTL function could be elicited in each subpopulation by exposure to non-infectious viral Ag.
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8

Kiziroglu, F., and R. G. Miller. "In vivo functional clonal deletion of recipient CD4+ T helper precursor cells that can recognize class II MHC on injected donor lymphoid cells." Journal of Immunology 146, no. 4 (February 15, 1991): 1104–12. http://dx.doi.org/10.4049/jimmunol.146.4.1104.

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Abstract Intravenous injection of semiallogeneic (C57BL/6XDBA/2)F1 lymphocytes into adult C57BL/6 recipient mice not only, as previously reported, reduces the recipients' cytotoxic T lymphocyte response in a subsequent in vitro mixed lymphocyte reaction against the injected cell type, but also reduces Th cell function in the same MLR. Thus lymphoid cells derived from the injected mice were greatly reduced in their ability to proliferate and to produce IL-2 in response to (C57BL/6XDBA/2)F1 stimulator cells in vitro, whereas third party responses were unaffected. This appears to be due to a reduction in the precursor frequency of IL-2-producing T lymphocytes specific for the injected cells as measured by limiting dilution analysis. Similar donor-specific reduction in the frequency of precursors of IL-2-producing cells was seen after i.v. injection of A.TL lymphocytes into A.TH recipients (differing at class II determinants I-A and I-E, but identical at K and D). Here there also appeared to be a functional clonal deletion of precursors of IL-2-producing Th cells, shown directly to be class II MHC reactive and CD4+. There is strong evidence that the reduction of class I-specific cytotoxic responses in the injected mice is a manifestation of donor cells that function as veto cells, i.e., that function as deletional APC that inactivate class I-reactive CTL precursors that recognize them. Our data in this study show that class II-specific Th responses are similarly reduced in the injected mice and suggest that CD4+ class II-reactive precursors of Th cells may be functionally inactivated in vivo by donor cells via a veto-like mechanism.
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9

Janssen, O., C. Nerl, and D. Kabelitz. "T cells in B-cell chronic lymphocytic leukemia: quantitative assessment of cytotoxic and interleukin-2-producing lymphocyte precursors by limiting dilution analysis." Blood 73, no. 6 (May 1, 1989): 1622–26. http://dx.doi.org/10.1182/blood.v73.6.1622.1622.

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Abstract Controversy exists as to the functional capacity of T lymphocytes in patients with B-cell chronic lymphocytic leukemia (CLL). We have used a limiting dilution (LD) culture approach to quantitatively assess frequencies of proliferating lymphocyte precursors (PLP), cytotoxic lymphocyte precursors (CLP), and interleukin-2 (IL-2)-producing helper lymphocyte precursors (HLP). Unseparated mononuclear cells (MNC) or purified T cells (E+) and leukemic B cells (E-) were cocultured under LD conditions with irradiated OKT3 hybridoma cells in the absence (determination of HLP) or presence of recombinant IL-2 (determination of PLP and CLP). Under these conditions, low frequencies of PLP, HLP, and CLP (f = 1/65 to 1/4600) were measured in unseparated MNC of CLL patients. In contrast, purified T cells (50% to 92% CD3+) contained precursors of proliferating, IL-2-producing and cytotoxic T cells in similar frequency as did T cells from healthy control donors (f = 1/4 to 1/24). Leukemic B cells rigorously depleted of T cells did not give rise to measurable frequencies of PLP, HLP, or CLP (f less than 1/50.000) except in one CLL patient where a significant frequency (f = 1/1700) of HLP was consistently present in E- cells, despite the absence of growth-inducible PLP and CLP. Taken together, these results indicate that comparable numbers of IL-2-producing helper T cells and cytotoxic T cells are present in B-CLL patients and healthy controls, respectively. The data are discussed with respect to reported T cell abnormalities in B-CLL.
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10

Janssen, O., C. Nerl, and D. Kabelitz. "T cells in B-cell chronic lymphocytic leukemia: quantitative assessment of cytotoxic and interleukin-2-producing lymphocyte precursors by limiting dilution analysis." Blood 73, no. 6 (May 1, 1989): 1622–26. http://dx.doi.org/10.1182/blood.v73.6.1622.bloodjournal7361622.

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Анотація:
Controversy exists as to the functional capacity of T lymphocytes in patients with B-cell chronic lymphocytic leukemia (CLL). We have used a limiting dilution (LD) culture approach to quantitatively assess frequencies of proliferating lymphocyte precursors (PLP), cytotoxic lymphocyte precursors (CLP), and interleukin-2 (IL-2)-producing helper lymphocyte precursors (HLP). Unseparated mononuclear cells (MNC) or purified T cells (E+) and leukemic B cells (E-) were cocultured under LD conditions with irradiated OKT3 hybridoma cells in the absence (determination of HLP) or presence of recombinant IL-2 (determination of PLP and CLP). Under these conditions, low frequencies of PLP, HLP, and CLP (f = 1/65 to 1/4600) were measured in unseparated MNC of CLL patients. In contrast, purified T cells (50% to 92% CD3+) contained precursors of proliferating, IL-2-producing and cytotoxic T cells in similar frequency as did T cells from healthy control donors (f = 1/4 to 1/24). Leukemic B cells rigorously depleted of T cells did not give rise to measurable frequencies of PLP, HLP, or CLP (f less than 1/50.000) except in one CLL patient where a significant frequency (f = 1/1700) of HLP was consistently present in E- cells, despite the absence of growth-inducible PLP and CLP. Taken together, these results indicate that comparable numbers of IL-2-producing helper T cells and cytotoxic T cells are present in B-CLL patients and healthy controls, respectively. The data are discussed with respect to reported T cell abnormalities in B-CLL.
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Більше джерел

Дисертації з теми "Lymphocyte precursors"

1

Jacobsen, Karen Ann. "Microenvironmental organization of B lymphopoiesis in mouse bone marrow : in vivo localisation of B lymphocyte precursors, molecular-interactions with stromal reticular cells, and macrophage-mediated deletion of apoptotic forms." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41346.

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The localisation of B lymphocyte precursor cells in mouse bone marrow and their associations with stromal reticular cells and macrophages have been investigated by in vivo radioimmunolabeling combined with light and electron microscope radioautography. Many early B lineage cells expressing the B220 glycoprotein prior to the expression of surface immunoglobulin and those regenerating after sub-lethal $ gamma$-irradiation, were located in bone-associated regions of femoral marrow. Labeled B220$ sp*$ lymphoid cells of undifferentiated morphology were closely associated with complex cytoplasmic processes of stromal reticular cells. The binding of a monoclonal antibody raised against a B lymphocyte-supportive stromal cell line (mAb KMI6), was highly restricted to the interface between stromal cells and undifferentiated lymphoid cells. The VCAM-1 specific mAb M/K-2, labeled electron-dense stromal cells that contacted lymphoid cells and a variety of other hemopoietic cell lineages. Within the bone marrow of normal mice there was evidence of death of B220$ sp+$ B lineage cells by apoptosis and their removal by macrophages. Cell loss, apoptosis and macrophage deletion of B precursor cells were greatly enhanced in E$ mu$-myc transgenic mice. The results reveal a complex in vivo microenvironmental organisation of B lymphocytopoiesis characterised by intimate interactions with stromal reticular cells and macrophages which regulate the development of precursor B cells and determine the ultimate output of B lymphocytes from the bone marrow.
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2

Ellabban, Wael. "Studies on precursors of human intestinal intraepithelial lymphocytes." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289072.

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3

Parker, Mathew James David. "Control of growth and performance of precursor B lymphocytes." Thesis, University of Cambridge, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614676.

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4

Kaminski, Eduardo Roman. "Cytotoxic T lymphocyte precursor frequencies (CTL-p) and their relevance to bone marrow transplantation." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46378.

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5

Liu, Jing. "Regulation of VH replacement in human immature B cells by B cell receptor (BCR)-mediated signaling." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010p/liu.pdf.

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6

D'ARGEMONT, CATHERINE. "La beta-2-microglobuline : un facteur chimiotactique pour les precurseurs des lymphocytes t." Paris 6, 1990. http://www.theses.fr/1990PA066464.

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Nous avons etudie les mecanismes controlant la colonisation du thymus par les cellules precurseurs des lymphocytes t chez les mammiferes en considerant l'hypothese selon laquelle l'epithelium thymique secrete des facteurs chimiotactiques capables d'attirer les precurseurs hematopoietiques medullaires. Le surnageant de la lignee epitheliale thymique de rat it45-r1 contient une proteine chimiotactique, baptisee thymotaxine, capable d'attirer in vitro des cellules de moelle osseuse de rat presentant des caracteristiques de cellules lymphoides immatures susceptibles de se differencier en lymphocytes t. La frequence de ces cellules dans la moelle osseuse de rat a ete evalue a 0. 015%. L'etude biochimique de la thymotaxine a revele son identite avec la beta-2-microglobuline (b2m). Cette proteine exerce son activite chimiotactique a une concentration optimale de 10##1#1m, qu'elle soit d'origine plasmatique ou recombinante. La b2m etant la chaine legere du complexe majeur d'histocompatibilite de classa i (cmh i), il nous a semble interessant d'utiliser la lignee it45-r1 pour etudier les mecanismes de production de cette proteine par des cellules exprimant les antigenes du cmh i. La secretion de b2m par ces cellules est constitutive, ne depend pas du taux d'expression du cmh i mais est due a une suspension de b2m intracellulaire et des transcrits codant pour cette proteine. A l'aide de cultures lymphoides, nous avons pu montre que l'un des evenements precoces induits par l'addition de b2m sur ces cellules est une augmentation de la concentration de calcium libre intracellulaire dependante d'un infux calcique. D'autre part, des resultats preliminaires indiquent que la b2m agirait grace a un recepteur membranaire specifique de 58 kd. L'expression de cette molecule par les cellules medullaires en culture mais pas par les thymocytes ou les cellules de moelle osseuse fraiche suggere une distribution cellulaire de ce recepteur differente de celle des antigenes du cmh i
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7

DOUAGI, IYADH. "Etude de l'engagement des precurseurs hematopoietiques et de leur differenciation en lymphocytes t et nk." Paris 6, 2001. http://www.theses.fr/2001PA066080.

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Анотація:
Les cellules qui composent le systeme hematopoietique presentent la particularite d'etre en constant renouvellement a partir de cellules souches hematopoietiques (csh) pendant toute la vie d'un individu. L'etude de ce systeme presente donc un interet majeur pour la comprehension des mecanismes cellulaires et moleculaires regissant l'engagement des precurseurs hematopoietiques dans les diverses voies de differenciations. De fait, la connaissance de la hierarchie ainsi que des precurseurs intermediaires entre la cellule souche et les cellules differenciees sont des pre-requis pour cette etude. Dans l'objectif de mieux comprendre ces mecanismes, nous avons focalise nos efforts a la caracterisation des precurseurs des lymphocytes t et nk. Nous avons montre qu'une fois dans le foie ftal, les precurseurs t proliferent avant de migrer probablement vers le thymus pour y subir les ultimes etapes de maturation. En parallele, nous avons observe qu'apres le stade 12 dpc, le thymus est colonise par nombre croissant de precurseurs nettement plus efficaces dans la generation de lymphocytes t que les premiers progeniteurs ayant colonise l'ebauche thymique. Cette conclusion, nous a conduit a envisager un scenario selon lequel le programme de differenciation vers la lignee t serait initie au niveau du foie ftal, avant l'arrivee de ces precurseurs t dans le thymus. De fait, l'analyse du potentiel de differenciation in vitro de differentes populations triees de cellules du foie ftal au stade 15 dpc nous a permis de montrer que la majorite des precurseurs t present dans cet organe etaient des precurseurs bipotent restreints aux lignees t et nk. Enfin, nous avons etendu notre etude a la caracterisation des precurseurs de cellules nk au niveau de la moelle osseuse adulte, ou nous avons identifie une population de progeniteurs engages vers la voie de differenciation nk.
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8

Maddila, Santhosh Chandar [Verfasser]. "Regulation of the opioid precursor proopiomelanocortin in lymphocytes in a rat model of inflammatory pain / Santhosh Chandar Maddila." Gießen : Universitätsbibliothek, 2015. http://d-nb.info/1068921897/34.

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9

Rizzuto, Gabrielle Ann. "Self-antigen specific CD8+ T cell precursor : frequency determines the quality of the anti-tumor immune response /." Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1621818951&sid=3&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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10

Abduh, Maisa. "Follicular CD4 T Cells Tutor CD8 Early Memory Precursors : an Initiatory Journey to the Frontier of B Cell Territory." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS371.

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Анотація:
Les lymphocytes T CD8+ spécifiques de l'antigène sont impliqués dans la réponse immunitaire adaptative et jouent un rôle essentiel dans la protection de l'hôte contre l'infection par des pathogènes intracellulaires. Cette protection de longue durée dépend de la génération de réponses lymphocytaires T CD8+ mémoires, hautement fonctionnelles en termes de fréquence et de fonctionnalité, après réinfection.Après présentation de l'antigène, une cellule T CD8 naïve subit une forte expansion clonale, générant une population hétérogène de cellules activées qui est dominée, au sommet de l'expansion, par des effecteurs CD8 de courte durée (SLEC). Cette expansion est suivie d'une phase de contraction massive par apoptose. Quelques cellules survivent à cette phase de contraction et finissent par se différencier en cellules mémoire hautement compétentes. Les processus par lesquels et le moment où se différencient les précurseurs de mémoire (MPECs) restent largement inconnus, tout comme les étapes ultérieures de leur maturation en cellules mémoire pleinement fonctionnelles. Les signaux d'aide provenant des cellules T CD4+ sont clairement requis tout au long du processus de maturation des MPEC.Notre équipe a montré que les lymphocytes T CD4+ régulateurs FoxP3+ (Tregs) favorisent la maturation des MPEC en limitant l'exposition à l'IL-2 et en fournissant des signaux inhibiteurs, mais ce n'est probablement qu'une facette de l'aide complexe et multiforme apportée par les cellules T CD4+ au MPEC. Les Tregs agissent sur des MPEC préexistants. Les réponses mémoire B et CD8+ partagent des caractéristiques communes, telles que l'expression du facteur de transcription Bcl-6. Les lymphocytes T CD4+ folliculaires (Tfh) sont les principaux producteurs de la cytokine IL-21. Bien que les mécanismes par lesquels les Tfh induisent l’expression de Bcl-6 dans les cellules B doivent être clarifiés, ils pourraient inclure l’IL-21 et l’interaction CD40-CD40L.Dans ce projet de thèse, nous avons étudié le rôle potentiel des Tfh dans l'initiation de la différenciation mémoire T CD8+, dans des modèles de souris transgéniques permettant une déplétion transitoire et sélective des Tfh, infectées par la bactérie recombinante Listeria monocytogenes-OVA.Nous avons montré que dès 2 jours après l'infection, les MPECs très précoces peuvent être identifiés par l’expression du récepteur de chimiokine CXCR5. Ces précurseurs précoces, qui ont un phénotype effecteur, se développent et migrent temporairement à la jonction des zones T et B, où ils interagissent avec les Tfh puis perdent leur expression CXCR5.Cette interaction avec les Tfh, considérés jusqu'à présent comme des auxiliaires exclusifs des cellules B, est nécessaire pour que les MPECs CD8+ deviennent des cellules mémoire compétentes sensibles à l'IL-21, capables de générer des réponses effectrices secondaires efficaces.Cette étude dévoile les premières étapes cruciales dans la génération de la mémoire CD8+, identifie CXCR5 comme le premier marqueur connu des MPECs CD8+, révèle l’implication fondamentale des Tfh dans le CD4 help et indique une coordination possible, via les Tfh, entre les voies de différentiation mémoire CD8+ et B. Ces résultats peuvent avoir des implications pour la conception du vaccin et de l'immunothérapie
Antigen-specific CD8 T cells are involved in the adaptive immune response and play a critical role in protecting the host from infection by intracellular pathogens. This long-lasting protection depends on the generation of memory CD8+ T cell responses, which are highly functional in terms of frequency and functionality, after secondary infection.Following antigen activation, a naive CD8 T cell undergoes strong clonal expansion, generating a heterogeneous population of activated cells that is dominated, at the peak of expansion, by short-lived CD8 effectors (SLECs). This expansion is followed by a phase of drastic contraction through massive apoptosis. A few cells survive this contraction phase and eventually become highly competent memory cells. Precisely when and how these memory precursors (MPECs) are generated is largely unknown, and so are the subsequent steps of their maturation into fully functional memory cells. Help signals from CD4+ T cells are clearly required throughout the MPEC maturation process.Our team has previously shown that FoxP3+ regulatory CD4+ T cells (Tregs) favor MPECs maturation by limiting exposure to IL-2 and by providing inhibitory signals, but this is probably only one facet of the complex and multifaceted help provided by CD4+ T cells to MPEC, and Tregs act on pre-existing MPECs.B-cell memory and CD8+ T cell memory share some common features, such as the expression of the transcription factor Bcl-6. Tfh are major producers of the cytokine IL-21. The mechanisms by which Tfh induces Bcl-6 in B-cells need to be clarified, they might include IL-21 and CD40-CD40L.In this PhD project, we have investigated the potential role of Tfh on the initiation of CD8 memory differentiation, in transgenic mice models, allowing transient and selective depletion of Tfh cells, infected by recombinant Listeria monocytogenes-OVA.We have shown that as early as 2 days after infection, very early memory precursors can be identified by their expression of the chemokine receptor CXCR5. These early precursors, which have an effector phenotype, expand and temporarily migrate to the junction of T-cell and B-cell zones, where they interact with follicular CD4 T cells (Tfh) then lose their CXCR5 expression.Remarkably, this interaction with Tfh, hitherto considered as exclusive B-cell helpers, is required for memory precursors to become competent memory cells responsive to IL-21 and capable of mounting efficient cytotoxic secondary effector responses.This study thus unveils critical early steps in the generation of CD8 memory, identifies CXCR5 as the earliest known marker of CD8 memory precursors, reveals a major helper role for Tfh, and points to possible coordination, through Tfh, between the pathways of CD8 and B-cell memory generation. These findings may have implications for vaccine and immunotherapy design
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Книги з теми "Lymphocyte precursors"

1

Woodward, Jeremy Mark. A study of lymphocyte precursors within the murine intestinal epithelium. Birmingham: University of Birmingham, 2000.

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2

Peter, Gale Robert, and Hoelzer Dieter, eds. Acute lymphoblastic leukemia: Proceedings of a Wyeth-Ayerst-UCLA Western Workshop--Acute Lymphoblastic Leukemia, held at Tapatio Springs, Texas, November 29-December 2, 1988. New York: Wiley-Liss, 1990.

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3

Bahiru, Gametchu, ed. Glucocorticoid receptor structure and leukemic cell responses. New York: Springer-Verlag, 1995.

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4

Secker-Walker, Lorna M. Chromosomes and genes in acute lymphoblastic leukemia. New York: Springer, 1997.

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5

Martin, Diego Raul *. Experimental studies of a potential immune tolerance mechanism that functionally deletes cytotoxic T lymphocyte precursors in adult mice. 1991.

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6

Bunch, Chris. Chronic leukaemia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0287.

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In the chronic leukaemias, leukaemogenesis occurs in two different cell types (and possibly even two different anatomical sites), leading to two very different forms of the disease: chronic myeloid leukaemia and chronic lymphocytic leukaemia. Chronic myeloid leukaemia is best thought of as a myeloproliferative disorder. It is a clonal disorder of the haematopoietic stem cell, leading to overproduction of the myeloid cells: neutrophils and their precursors, basophils and eosinophils. By contrast, chronic lymphocytic leukaemia can be viewed as a low-grade lymphoma. It is a clonal disorder of mature B-lymphocytes (possibly memory B-cells). This chapter reviews the causes, diagnosis, and management of these two forms of chronic leukaemia.
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7

I Never Signed Up for This!: An Upfront Guide to Dealing with Cancer at a Young Age. PublishAmerica, 2006.

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8

(Editor), Robert Peter Gale, and Dieter Hoelzer (Editor), eds. Acute Lymphoblastic Leukaemia (UCLA symposia on molecular and cellular biology). John Wiley & Sons Inc, 1990.

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Частини книг з теми "Lymphocyte precursors"

1

Kincade, Paul W., Kay Medina, Glennda Smithson, Zhong Zheng, Kenji Oritani, Lisa Borghesi, Yoshio Yamashita, Kimberly Payne, and Takaichi Shimozato. "Life/Death Decisions in B Lymphocyte Precursors." In Molecular Biology of B-Cell and T-Cell Development, 177–96. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-4757-2778-4_10.

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2

Piantelli, S., G. Maccauro, P. Fassina, and A. Bukat. "Effect of TiO2 Ceramic Precursors on Human Lymphocyte Mitogenesis." In Bioceramics and the Human Body, 378–82. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2896-4_52.

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3

Müller-Sieburg, C. E., N. Martina, and J. P. Wineman. "Pluripotent Stem Cells and Early B Lymphocyte Precursors in Mice." In Current Topics in Microbiology and Immunology, 107–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76912-2_9.

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4

Lee, G., A. E. Namen, S. Gillis, and P. W. Kincade. "Recombinant Interleukin-7 Supports the Growth of Normal B Lymphocyte Precursors." In Current Topics in Microbiology and Immunology, 16–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_3.

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5

Imhof, B. A., M. A. Deugnier, T. Itoh, and J. P. Thiery. "T Lymphocyte Precursors Migrate Towards Chemotactic Peptides Secreted by Embryonic or Juvenile Thymus." In Advances in Experimental Medicine and Biology, 565–70. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5535-9_86.

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6

Melchers, Fritz, Dirk Haasner, Martin Streb, and Antonius Rolink. "B-Lymphocyte Lineage-Committed, IL-7 and Stroma Cell- Reactive Progenitors and Precursors, and Their Differentiation to B Cells." In Advances in Experimental Medicine and Biology, 111–17. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3396-2_14.

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7

Wagner, H., and C. Hardt. "Heterogeneity of the Signal Requirements During the Primary Activation of Resting Lyt-2+ Cytotoxic T-Lymphocyte (CTL) Precursors into Clonally Developing CTL." In Current Topics in Microbiology and Immunology, 143–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71152-7_18.

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8

Melchers, F. "B-lymphocyte-lineage Cells from Early Precursors to Ig-secreting Plasma Cells: Targets of Regulation by the myc/mad/max Families of Genes?" In Current Topics in Microbiology and Immunology, 19–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60801-8_2.

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9

Ceredig, R. "Major Histocompatibility-Restricted Cytolytic T-Lymphocyte Precursors from the Thymus of In Vivo Primed Mice: Increased Frequency and Resistance to Anti-Lyt-2 Antibody Inhibition." In Current Topics in Microbiology and Immunology, 27–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71152-7_4.

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10

Melchers, Fritz, Steven R. Bauer, Christoph Berger, Hajime Karasuyama, Akira Kudo, Antonius Rolink, Nobuo Sakaguchi, Andreas Strasser, and Philipp Thalmann. "Precursor B Lymphocytes — Specific Monoclonal Antibodies and Genes." In Mechanisms of Lymphocyte Activation and Immune Regulation II, 87–93. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-5803-0_11.

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Тези доповідей конференцій з теми "Lymphocyte precursors"

1

Cavalcante, Jéssica Moreira, Mauro Henrique Muniz Goursand, Douglas de Miranda Pires, Paula Clarke, and Fernanda Silveira de Oliveira. "LYMPHOCYTIC MASTOPHATY PRECEDING BILATERAL PRIMARY BREAST LYMPHOMA – CASE REPORT." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1011.

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Introduction: Lymphocytic mastopathy is a rare condition, responsible for 1% of all benign breast lesions, commonly associated to autoimmune disorders and diabetes (especially insulin-requiring diabetes). The differential diagnosis may be difficult, since the clinical and imaging aspects can mimic malignant disease. Some authors suggest that lymphocytic mastitis could be a precursor of primary breast lymphoma. However, other studies disagree with such correlation, presenting the mastopathy as a distinct diagnosis, but one of difficult differentiation from lymphoma. To avoid misdiagnosis, an appropriate study of the specimen is recommended, through image-guided or surgical biopsy and immunohistochemical markers. Due to its unique presentation and scarce reports in global literature, we present a case of a patient with lymphocytic mastopathy that preceded the diagnosis of primary bilateral lymphoma. Case report: A healthy 46-year-old, nulliparous, premenopausal female patient, with a negative family history of breast cancer, presented palpable masses in the inferior medial quadrants (IMQ) of the right and left breasts, measuring 5 cm and 1.2 cm, respectively, both classified as Category 4 in the BIRADS lexicon. She was referred for excisional surgical biopsy, with anatomopathological diagnosis compatible with nonspecific chronic mastitis in both specimens. Immunohistochemistry (IHC) revealed lymphocytic mastitis, without signs of malignancy. The patient maintained regular control with a mastologist and after two years of follow-up, two new category 4 masses were identified: one in the IMQ of the right breast, and another in the retro-areolar (RRA) region of the left one. Core biopsy of the masses revealed lymphoproliferative disease, with IHC showing non-Hodgkins’ diffuse large B-cell lymphoma, (Ki67 60%, CD20+, BCL6+). A magnetic resonance imaging of the breasts identified bilateral breast masses in the RRA region, with extension to the medial quadrants and no cleavage plane with the nipple, the largest measuring 4.5 cm, in the left breast, with heterogeneous internal enhancement and type III kinetic pattern, in addition to an atypical lymph node in level I of the right axilla. Positron emission tomography–computed tomography (PET-CT) ruled out distant disease, and confirmed it was restricted to the breasts. The patient received six cycles of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone, presenting a complete metabolic response on PET-CT. Subsequently, radiotherapy was performed on both breasts at a dose of 30 Grays in 15 fractions each and, after a clinical follow-up of two months, no new abnormalities have been noted.
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Kieffer, N., L. Edelman, P. Edelman, C. Legrand, J. Breton-Gori us, and W. Vainchenker. "A MONOCLONAL ANTIBODY AGAINST AN ERYTHROID ONTOGENIC ANTIGEN IDENTIFIES GP IV ON HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643532.

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A murine monoclonal antibody (FA6-152), obtained by immunizing mice with fetal human erythrocytes agglutinated fetal but not adult erythrocytes and bound to both adultand fetal monocytes, platelets andreticulocytes. The antibody did not react with lymphocytes or granulocytes (P. Edelman et al., Blood, 1986, 67, 56). Fluorescent labeling of marrow cells and of in vitro BFU-E, CFU-GM and CFU-MK derivedcolonies revealed that the antigen defined by FA6 was absent from the granulocytic precursors and was detected on the megakaryo-cytic lineage at a later stage of differentiation than major platelet membraneglycoprotein markers. In contrast,the antigen appeared as a very early marker of erythroid differentiation.In the present report, we performed immunoprecipitation experiments on surface labeled platelets toidentify the platelet FA6 antigen.A band of apparent Mr - 85,000 wasimmunoprecipitated from iodinated platelets. This band was also revealed after periodate/Na[3H]BH4 orneuraminidase galactose oxidase/Na[3H]BH4 surface labeling of the platelets, providing evidence that the FA6 antigen corresponds to platelet GP IV. Preliminary studies revealed that FA6-IgG inhibited platelet aggregation induced by low doses of thrombin without affecting the platelet release reaction. Our results therefore suggest that GP IV, which isa multi-lineage hematopoietic differentiation marker, could play a role in cell-cell or cell-substrateinteractions common to different hematopoietic cell types.
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Cramer, Elisabeth M., F. John, William Vainchenker, and Janine Breton-Gorius. "PRODUCTION AND LOCALISATION OF ALPHA-GRANULE PROTEINS IN MATURING MEGAKARYOCYTES: AN OVERVIEW ON ULTRA-STRUCTURAL ASPECTS OF MEGAKARYOCYTE MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642952.

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In order to study the production of α- granule proteins in maturing megakaryocytes, we used immunocytochemical techniques performed on cultured and enriched bone marrow megakaryocytes. Cultures were prepared from bone marrow CFU-MK with the methylcellulose and plasma clot techniques. Preparation of bone marrow megakaryocytes was carried out from human or pig rib marrow separated on percoll gradient and counterflow centrifugation. Megakaryocyte preparations were 90$ pure and represented 85$ of those in the whole marrow. Activation was prevented with prostacyclin and prefixation with low concentration glutaraldehyde. A panel of monoclonal and polyclonal antibodies, against different platelet membrane glycoproteins and against cytoplasmic antigens (such as von Willebrand Factor (vWF), fibrinogen (Fg) and thrombospondin (TSP)) was used and observed by immunofluorescence or by immunogold in electron microscopy.The first megakaryocytic precursors, promegakaryoblasts (PMKB) identifiable by these antibodies were found at day 5 of culture. They had the size of lymphocytes, were labelled for GP lib, Ilia, and Ilb-IIIa complex but not for GPIb which appeared later. Platelet peroxidase was also present, otherwise these cells were devoid of α- granules and only a few of them exhibited a diffuse pattern for vWF immunolabelling. One day later membrane GPIb and diffuse cytoplasmic labelling for vWF were detected in the majority of PMKB. At day 9 of culture, this pattern of labelling for vWF became more intense and granular. The same pattern was observed for TSP and platelet factor 4. Immunoelectron microscopy showed that in immature megakaryocytes isolated from human bone marrow, labelling for vWF and TSP was observed in vesicles located in the Golgi region; in addition numerous small granules less than 0.1pm in diameter, round or elongated in shape, were labelled for these antigens. In mature human megakaryocytes, the labelling for these cytoplasmic antigens was restricted to the platelet α- granules in a distribution pattern similar to that of platelet α- granules. However, the labelling for Fg was consistently less intense in the granules of immature and mature megakaryocytes than in platelets.Because in platelets α- granule immunolabelling for vWF is associated with tubular structures which are specially prominent in porcine species, we studied vWF and tubular structures in pig megakaryocytes. Standard and immunoelectron microscopy revealed the simultaneous appearance of both in the small vesicles located in the Golgi area in the small immature α- granules and later in the mature α- granules. In mature megakaryocytes, labelling for vWF was intense and restricted to the α- granules. It was distributed eccentrically as in porcine blood platelets. Gold particles were often eccentrically located at one pole of the α- granule either labelling only its periphery or outlining one side of an elongated granule. Standard electron microscopy showed that tubular structures were very numerous in the mature α-granules, regularly spaced, arranged in parallel and usually located at one side of the granule. On the other hand platelets from pigs with homozygous von Willebrand disease were found to be completely devoid of both tubular structures and immunolabelling for vWF suggesting that the tubules represent the vWF itself.In acute megakaryoblastic leukemia, several phenotypes of PMKB were found in different patients, which corresponded to the stages of maturation of cultured megakaryocytes from CFU-MK.In conclusion, immunolabelling methods combined with megakaryocyte enrichment techniques are useful tools to study the origin of megakaryocyte (and platelet) granular proteins.
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