Browsing by Subject "Bone Marrow Transplantation"
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Item Allogeneic bone marrow transplantation(2000-12-07) Collins, Robert, Jr.Item Allogeneic bone marrow transplantation: current obstacles and future prospects(1987-10-08) Thiele, Dwain L.Item Autologous bone marrow transplantation: climbing the dose-response curve(1989-03-30) Fleischman, Roger A.Item Bone marrow transplantation revisited(1977-08-25) Streilein, J. WayneItem Chronic granulocytic leukemia: the devastating consequences of genetic instability(1985-12-12) Smith, R. GrahamItem Development of a Human Immune System from Hematopoietic Stem Cells in a Human/Mouse Xenogeneic Model(2006-12-20) Melkus, Michael W.; Garcia-Martinez, J. VictorT cells play a central role in the development of immune responses. Patients lacking T cells due to genetic defects such as DiGeorge or Nezelof's syndrome and individuals infected with the human immunodeficiency virus are highly susceptible to infections and cancers. The lack of adequate in vivo models of T cell neogenesis has hindered the development and clinical implementation of effective therapeutic modalities aimed at treating these and other clinically important maladies. Transplantation of severe combined immunodeficient (SCID) mice with human hematopoietic stem cells results in long-term engraftment and systemic reconstitution with human progenitor, B and myeloid cells but curiously, human T cells are rarely present in any tissue. While the implantation of SCID mice with human fetal thymus and liver (SCID-hu thy/liv mice) allows for the development of abundant thymocytes that are localized to the human organoid implant, there is minimal systemic repopulation with human T cells. Here I present evidence that transplantation of autologous human hematopoietic fetal liver CD34+ cells into NOD/SCID mice previously implanted with fetal thymic and liver tissues results in long-term, systemic human T cell homeostasis. In addition to human T cells, these mice have systemic repopulation with human B cells, monocytes/macrophages and dendritic cells (DC). This mouse model of the human immune system has been designated as BLT for a Bone marrow transplant in fetal Liver and Thymus implanted mice. T cells in these mice generate human MHC Class I and Class II restricted adaptive immune responses to Epstein Barr virus infection and are activated by human DCs to mount potent T cell immune response to super antigens. Administration of the super-antigen toxic shock syndrome toxin-1 (TSST-1) resulted in the specific systemic expansion of human Vbeta 2+ T cells, release of human pro-inflammatory cytokines and localized specific activation and maturation of human CD11c+ dendritic cells. These results represent the first demonstration of long-term systemic human T cell reconstitution in vivo allowing for the manifestation of the differential response by human DCs to TSST-1.Item Lymphohematopoietic reconstitution(1972-03-23) Streilein, J. WayneItem [News](1992-02-20) Gentry, LynnItem Refining Our Understanding of the Hematopoietic Stem Cell Niche(2015-09-24) Peyer, James Gregory; DeBerardinis, Ralph J.; Morrison, Sean J.; Buszczak, Michael; Olson, Eric N.A major therapeutic goal of studying blood-forming hematopoietic stem cells (HSCs) is to understand the mechanisms by which HSCs are maintained in the bone marrow, so that they can be grown outside of the body and used in lieu of or in combination with bone marrow transplantation to treat hematopoietic illnesses. HSCs, as well as other somatic stem cells from different organ systems and organisms, rely on signals from their local microenvironment for their maintenance. However, the identity of the HSC niche is still poorly understood. One new model of the HSC niche is that HSCs, periarteriolar stromal cells, and nerve fibers are closely associated in rare periateriolar niches. Using a novel marker to identify HSCs in three-dimensional confocal images, -catulin-GFP, we measured the distances from thousands of HSCs to various landmarks in the bone marrow. We found that few HSCs are closely associated with either nerve fibers or arterioles. Mice lacking sympathetic nerves exhibit multiple changes in hematopoiesis, especially in response to injury, though all of the studies published so far have systemically ablated sympathetic nerves. This left unresolved the question of whether the changes in hematopoiesis reflect bone marrow denervation itself, or systemic effects of general sympathectomy. To test this, I developed a model for bone marrow-specific neuropathy by conditionally deleting nerve growth factor (Ngf) from bone marrow stromal cells. Using this model, I analyzed the role of bone marrow peripheral nerves in hematopoiesis. I demonstrated that while nerves play no role in bone marrow homeostasis, nerve signaling after bone marrow injury is essential for hematopoietic regeneration. Future studies will build on this work to understand how nerve fibers promote the regeneration of HSCs and bone marrow cells despite not innervating the HSC niche themselves.Item Role of autologous bone marrow transplantation in the treatment of human malignancies(1997-11-06) Gaynor, Richard B.Item [Southwestern News](2001-03-01) Morrison, SusanItem [Southwestern News](2003-02-04) Maier, ScottItem [UT Southwestern Medical Center News](2008-04-24) Piloto, Connie