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Pathologe. 2002 Nov;23(6):405-10. Epub 2002 Oct 09.
[Chimerism of cardiomyocytes and endothelial cells after allogeneic bone marrow transplantation in chronic myeloid leukemia. An autopsy study]

[Article in German]

Thiele J, Varus E, Wickenhauser C, Kvasnicka HM, Metz K, Schaefer UW, Beelen DW.

Zentrum fur Pathologie, Universitat zu Koln, Joseph-Stelzmann-Strasse 9, 50924 Koln, Germany. j.thielni-koeln.de

The results of a number of animal experimental studies are in keeping with the finding that hematopoietic progenitors can generate cardiomyocytes and endothelial cells. As a consequence innovative therapeutic strategies have been suggested to possibly ameliorate the outcome of coronary artery disease. However, there is no information available at present whether this pathomechanism is also effective in humans, in particular without prior ischemic lesion of the myocardium. Therefore an autopsy study was performed on cadaver hearts derived from five male patients with chronic myeloid leukemia who received full unmanipulated bone marrow grafts from female donors 21-631 days before death. The purpose of this investigation was to detect and quantify a putative chimerism of cardiomyocytes and endothelial cells (intramural and subepicardial vessels). Genotyping was carried out by applying X- or Y-chromosome-specific DNA probes (fluorescence in-situ hybridisation) on routinely formalin-fixed specimens of the myocardium. To test the sensitivity of our method, cadaver hearts from two males and two females without a history of transplantation served as controls. In contrast to a totally corresponding sex-matched genotyping in 780 cardiomyocytes and 155 endothelial cells of the control group, the five male patients with a previous transplantation revealed significantly different results. A mixed chimerism was identifiable in 57 out of 890 counted cardiomyocytes (6.4%) and in 19 out of 322 endothelial cells (5.8%). These findings support the assumption that in addition to endothelial cells there is also a cardiomyogenic potential of bone marrow stem cells which exists without prior (ischemic) damage to the heart. However, further investigations are necessary to identify, isolate and enrich the cardiomyocytic stem cells more specifically for future curative therapeutic options in patients with severe ischemic cardiomyopathy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12436292&dopt=Abstract

Blood. 2002 Jun 1;99(11):4030-8.
Normal hemostasis but defective hematopoietic response to growth factors in mice deficient in phospholipid scramblase 1.

Zhou Q, Zhao J, Wiedmer T, Sims PJ.

Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.

Phospholipid scramblase 1 (PLSCR1) is an endofacial plasma membrane protein proposed to participate in transbilayer movement of phosphatidylserine and other phospholipids. In addition to its putative role in the reorganization of plasma membrane phospholipids, PLSCR1 is a substrate of intracellular kinases that imply its possible participation in diverse signaling pathways underlying proliferation, differentiation, or apoptosis. Because PLSCR1 is prominently expressed in a variety of blood cells, we evaluated PLSCR activity in platelets and erythrocytes, and cytokine-dependent growth of hematopoietic precursor cells, of PLSCR1 knock-out mice. Adult PLSCR1(-/-) mice showed no obvious hematologic or hemostatic abnormality, and blood cells from these animals normally mobilized phosphatidylserine to the cell surface upon stimulation. Whereas blood cell counts in adult PLSCR1(-/-) mice were normal, in both fetus and newborn animals neutrophil counts were significantly depressed relative to age-matched wild type (WT). Furthermore, when compared with WT, hematopoietic precursor cells from PLSCR1(-/-) mice showed defective colony formation and impaired differentiation to mature granulocytes as stimulated by stem cell factor and granulocyte colony-stimulating factor (G-CSF). By contrast, PLSCR1(-/-) cells showed normal colony formation stimulated by interleukin-3 or granulocyte-macrophage CSF, and expansion of megakaryocytic and erythroid progenitors by thrombopoietin or erythropoietin was unaffected. Stem cell factor and G-CSF were also found to induce marked increases in PLSCR1 levels in WT cells. Consistent with in vitro assays, PLSCR1(-/-) mice treated with G-CSF showed less than 50% of the granulocytosis observed in identically treated WT mice. These data provide direct evidence that PLSCR1 functionally contributes to cytokine-regulated cell proliferation and differentiation and suggest it is required for normal myelopoiesis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010804&dopt=Abstract

Blood. 2002 Jun 1;99(11):4053-62.
Defective T-helper cell function after T-cell-depleting therapy affecting naive and memory populations.

Heitger A, Winklehner P, Obexer P, Eder J, Zelle-Rieser C, Kropshofer G, Thurnher M, Holter W.

University Children's Hospital Innsbruck; Department of Urology, University Innsbruck, Austria. andreas.heitgeibk.ac.at

Impaired T-cell function after T-cell- depleting (TCD) therapy has been hypothesized to be related to a transient predominance of extrathymically expanding memory T cells. To test whether after TCD therapy the naive T-helper cell population is functionally intact, the in vitro immune response of CD4(+)CD45RA(+) (naive) and of CD4(+)CD45RA(-) (memory) cells to polyclonal mitogens (immobilized anti-CD3, phytohemagglutinin) was analyzed by flow cytometry in 22 pediatric patients after high-dose chemotherapy (including 5 after autologous and 5 after allogeneic stem cell support). At 1 to 3 months after TCD therapy, patient samples showing decreased lymphoproliferative responses also showed a reduced induction of the early activation marker CD69 by CD4(+) T cells from 4 to 72 hours after stimulation even when supplemented with exogenous interleukin-2. This defect affected CD4(+)CD45RA(-) cells, but, strikingly, also CD4(+)CD45RA(+) cells, including samples in which CD4(+)CD45RA(+) cells were more than 90/microL, thus indicating ongoing thymopoiesis. Histogram analyses showed the median peak channel of CD69 in control CD4(+)CD45RA(+) cells rising 98-fold (median) but only 28-fold in patient cells (P <.0001). Apoptosis as detected by annexin V staining was increased in resting patient CD4(+) T cells (25% versus 6%) and also affected CD4(+)CD45RA(+) cells (12% versus 5%, P <.01). When peripheral blood mononuclear cells (PBMCs) were enriched for T cells, stimulatory responses of CD4(+) cells and of CD4(+)CD45RA(+) cells markedly improved. Thus, after TCD therapy suppressor factors contained in the non-T-cell fraction of PBMCs may affect T-helper cells irrespective of their naive or memory phenotype thus extending T-cell dysfunction to the presumably thymus-dependently regenerated T cells.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010807&dopt=Abstract

Blood. 2002 Jun 1;99(11):4174-81.
Tolerance induction by megadose hematopoietic progenitor cells: expansion of veto cells by short-term culture of purified human CD34(+) cells.

Gur H, Krauthgamer R, Berrebi A, Klein T, Nagler A, Tabilio A, Martelli MF, Reisner Y.

Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.

Stem cell-dose escalation is one way to overcome immune rejection of incompatible stem cells. However, the number of hematopoietic precursors required for overcoming the immune barrier in recipients pretreated with sublethal regimens cannot be attained with the state-of-the-art technology for stem cell mobilization. This issue was addressed by the observation that cells within the human CD34(+) population are endowed with veto activity. In the current study, we demonstrated that it is possible to harvest about 28- to 80-fold more veto cells on culturing of purified CD34(+) cells for 7 to 12 days with an early-acting cytokine mixture including Flt3-ligand, stem cell factor, and thrombopoietin. Analysis of the expanded cells with fluorescence-activated cell-sorter scanning revealed that the predominant phenotype of CD34(+)CD33(-) cells used at the initiation of the culture was replaced at the end of the culture by cells expressing early myeloid phenotypes such as CD34(+)CD33(+) and CD34(-)CD33(+). These maturation events were associated with a significant gain in veto activity as exemplified by the minimal ratio of veto to effector cells at which significant veto activity was detected. Thus, whereas purified unexpanded CD34(+) cells exhibited veto activity at a veto-to-effector cell ratio of 0.5, the expanded cells attained an equivalent activity at a ratio of 0.125. The availability of novel sources of veto cells such as those in this study might contribute to the realization of immunologic tolerance in "minitransplants," without any risk of graft-versus-host disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010823&dopt=Abstract

Blood. 2002 Jun 1;99(11):4200-6.
The clinical significance of human leukocyte antigen (HLA) allele compatibility in patients receiving a marrow transplant from serologically HLA-A, HLA-B, and HLA-DR matched unrelated donors.

Morishima Y, Sasazuki T, Inoko H, Juji T, Akaza T, Yamamoto K, Ishikawa Y, Kato S, Sao H, Sakamaki H, Kawa K, Hamajima N, Asano S, Kodera Y.

Department of Hematology and Chemotherapy, the Division of Epidemiology and Prevention, Aichi Cancer Center, Japan. ymorisiichi-cc.jp

To improve the clinical outcome of allogeneic hematopoietic stem cell transplantation from an unrelated donor, the identification of human leukocyte antigen (HLA) alleles responsible for immunologic events such as graft-versus-host disease (GVHD), engraftment failure, and graft-versus-leukemia effect is essential. Genomic typing of HLA-A, -B, -C, -DRB1, and -DQB1 was retrospectively performed in 1298 donor-patient pairs in cases where marrow was donated from serologically HLA-A, -B, and -DR compatible donors. Single disparities of the HLA-A, -B, -C, or -DRB1 allele were independent risk factors for acute GVHD, and the synergistic effect of the HLA-C allele mismatch with other HLA allele mismatches on acute GVHD was remarkable. HLA-A and/or HLA-B allele mismatch was found to be a significant factor for the occurrence of chronic GVHD. HLA class I (A, B, and/or C) allele mismatch caused a significantly higher incidence of engraftment failure than HLA match. Significant association of HLA-C allele mismatch with leukemia relapse was not observed. As the result of these events, HLA-A and/or HLA-B allele mismatch reduced overall survival remarkably in both standard-risk and high-risk leukemia cases, whereas the HLA-C mismatch or HLA-class II (DRB1 and/or DQB1) mismatch did not. Furthermore, multiple mismatch of the HLA locus was found to reduce survival in leukemia cases. Thus, the role of the HLA class I allele in unrelated bone marrow transplantation was elucidated. Notably, HLA-C alleles had a different mode from HLA-A or -B alleles for acute GVHD and survival.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12010826&dopt=Abstract

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