Factors regulating murine B lineage development
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Factors regulating murine B lineage development an in vitro analysis. by Craig Duncan Milne

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Published .
Written in English

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The complex process of B lineage cell development is controlled by many factors produced from the surrounding microenvironment. These factors can include cytokines, extracellular matrix molecules, chemokines, adhesion molecules, and cell-surface proteins that act in concert to regulate B lineage cells. In vitro assays have provided invaluable insights into the biology of many of these factors. This thesis focuses on new models of factors that regulate B lineage cells as they transit from progenitor cells to immuno-competent, BCR-expressing B cells. B cell progenitors require the cytokine interleukin-7 (IL-7) for survival, proliferation and maturation. Data contained herein contest a popular hypothesis that IL-7 also prevents maturation of progenitors to the BCR+ stage. These data also reveal that in vitro cultures of B lineage cells containing IL-7 are highly heterogeneous and some subpopulations within the culture proliferate, while others mature, or undergo apoptosis. The following sections of this thesis examine an undefined contact-dependent event that appears necessary for progenitor B cells to become responsive to lipopolysaccharide (LPS), an attribute of mature B cells. Previous models have relied upon co-culture systems employing stromal cells to mediate this transition. Data presented in this thesis reveal that stromal cells play accessory roles by attracting B lineage cells to sites of contact through the production of chemokines. Stromal cells also augment the survival of cells stimulated with LPS, but they are not necessary for cells to become LPS-responsive. Finally, data suggest that heparan sulfate can alter the maturation of progenitor cells and may play a role in mediating contact-dependent events between B lineage cells.

The Physical Object
Pagination211 leaves.
Number of Pages211
ID Numbers
Open LibraryOL21302846M
ISBN 100494077077

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The objective of this paper is to give a brief overview of our laboratory’s present activities utilizing a culture system which supports the longterm growth of cells restricted to the B-lymphocyte lineage. These studies are aimed at understanding the fundamental mechanisms involved in the normal development of B .   The formation of the trophoblast cell lineage of the placenta is one of the first developmental events to occur in mammalian embryogenesis. To understand the mechanisms of gene regulation in the trophoblast cell lineage we have used the murine adenosine deaminase gene (Ada) as a is highly expressed in trophoblast cells of the placenta and is critical for embryo by: 7. Several studies suggest that FcgammaR can influence leukocyte development and that FcgammaRII (CD32) and FcgammaRIII (CD16) can regulate murine T- and B-lineage development .   PHO2; stomatal development; stomatal lineage miRNA; Control of cell lineage and patterning plays a crucial role in the development of multicellular organisms (1 ⇓ –3).Transcription factors can act as master modulators of cell fate specification (2, 4).Environmental factors, including positional cues and neighboring cells, have also been shown to affect cell fate during development .

  While murine GTLM iEPs express both embryonic and adult globin genes, the addition of Klf1 or Myb induces a switch in globin gene expression to generate iEPs with a predominant definitive-type globin expression pattern. This approach can be used as a model for understanding, controlling, and recapitulating erythroid lineage development and disease.   1. Introduction. B lymphopoiesis within the bone marrow is compromised during senescence in a variety of inbred mouse strains,,,.Alterations affect multiple stages in B cell development including generation and maintenance of pro-B cells, pre-B cells, and immature B cells,,,.Several mechanisms have been proposed to contribute to the paucity in B lymphopoiesis seen in murine Cited by:   This review highlights recent advances concerning factors that govern early B cell development by modulating gene expression. Regulation in progenitors before B lineage specification: Ikaros, PU.1 and E2A. HSC multipotency derives from low-level expression of lineage-affiliated genes associated with multiple hematopoietic backgrounds [3, 4].   Inducible expression of reprogramming factors in the B cell lineage. Our initial strategy was to determine whether Oct4, Sox2, Klf4 and c-Myc transcription factors, which were shown to be sufficient to reprogram mouse and human fibroblast cultures (Meissner et al., ; Okita et al., ; Takahashi et al., ; Takahashi and Yamanaka, ; Wernig et al., ), were capable of.

Development of cell lineages ultimately involves changes in programs of gene expression, which are in turn regulated by transcription factors. A large number of transcription factors that are expressed in trophoblast have now been identified (Table ). Orkin S.H. () Transcription Factors Regulating Early Hematopoietic Development and Lineage Commitment. In: Monroe J.G., Rothenberg E.V. (eds) Molecular Biology of B-Cell and T-Cell Development. Contemporary Immunology.   B-cell maturation proceeds through distinct developmental stages that are largely characterized by the generation and modification of antibodies that function during adaptive immune responses (1 –3).This hierarchical development is controlled in part by the activation/inactivation of transcription factors (TF), resulting in the induction or suppression of large sets of genes that are.   These results imply that the anti-allergic effect of BV may arise from the direct regulation of helper T cell lineage programming via T-bet regulation. The role of other transcription factors associated with helper T cell development such as c-Maf, Stat6 and Stat4 in the presence of BV should be investigated to elucidate the detailed mechanisms.