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Yoshioka K Yamamoto S Moriguchi N Miyata H Tsukiyama K Isokawa S Horiuchi F Takemura T 《Annals of hematology》2000,79(6):319-321
Transient abnormal myelopoiesis (TAM) is a haematological complication found in Down syndrome. To determine the mechanisms
of sustained proliferation of TAM cells, we studied the expression of apoptosis-related proteins, such as bcl-2, Fas (APO-1/CD95) and p-53, in peripheral blood cells from a new-born infant with Down syndrome and TAM. Using flow cytometry, peripheral blood mononuclear
cells (PBMCs), consisting mostly of blast cells, showed marked expression of bcl-2 protein but not of Fas or p-53 products. DNA gel electrophoresis of PBMCs, cultured in the absence of serum factors, revealed no marked fragmentation. Our
findings suggest that bcl-2 overexpression may be associated with prolonged cell survival of TAM cells.
Received: 8 March 1999 / Accepted: 9 November 1999 相似文献
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Helena M Kempski Janet L Craze Judith M CHESSElls & Brian R Reeves 《British journal of haematology》1998,103(2):473-479
A case of transient abnormal myelopoiesis in a normal newborn without features of Down syndrome is described. The majority of bone marrow cells analysed belonged to a chromosomally abnormal clone with trisomy for chromosomes 18 and 21. Complex intrachromosomal rearrangements of one chromosome 21, demonstrated by fluorescence in situ hybridization using locus-specific probes, were found in a minor population of the clonal cells. These rearrangements involved loci previously shown to be rearranged in the leukaemic cells from patients with Down syndrome and leukaemia. However, the child's myeloproliferation resolved rapidly, with disappearance of the abnormal clone, and 3.5 years later she remains well. 相似文献
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《International reviews of immunology》2013,32(6):454-469
CD137 ligand (CD137L) has emerged as a powerful regulator of myelopoiesis that links emergency situations, such as infections, to the generation of additional myeloid cells, and to their activation and maturation. CD137L is expressed on the cell surface of hematopoietic stem and progenitor cells (HSPC) and antigen presenting cells (APC) as a transmembrane protein. The signaling of CD137L into HSPC induces their proliferation and differentiation to monocytes and macrophages, and in monocytes CD137L signaling induces differentiation to potent dendritic cells (DC). CD137L signaling is initiated by CD137 which is expressed by T cells, once they become activated. Some of these activated, CD137-expressing T cells migrate from the site of infection to the bone marrow where they interact with HSPC to induce myelopoiesis, or they induce monocyte to DC differentiation locally at the site of infection. Therapeutically, induction of CD137L signaling can be utilized to reinitiate myeloid differentiation in acute myeloid leukemia cells, and to generate potent DC for immunotherapy. 相似文献
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William M. Crist Abdelsalem H. Ragab Larry Vogler Victor K. S. Lui Robert P. Castleberry Harry W. Findley Greg Merijanian 《Pediatric blood & cancer》1980,8(3):289-294
Soft agar culture studies of 43 immunologically characterized patients with childhood acute lymphocytic leukemia (ALL) are presented. The immunologic subsets studied include “null”-cell, pre-B-cell, and T-cell leukemias. Abnormal myelopoiesis, including high peripheral blood and low marrow, colony-forming cell numbers, low colony-stimulating activity, and normal maturation of colony-forming cells in vitro was noted in each group as previously described for immunologically uncharacterized ALL. We conclude that immunologic subsets of childhood lymphoblastic leukemia cause similar abnormalities of myelopoiesis. Lack of differences in growth characteristics among immunologic subsets of ALL make it impossible to use this tissue culture technique in sub-classification of these leukemic disorders. 相似文献
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Karlsson J Carlsson G Ramme KG Hägglund H Fadeel B Nordenskjöld M Henter JI Palmblad J Pütsep K Andersson M 《British journal of haematology》2007,137(2):166-169
Chronic neutropenia comprises several different diseases that vary in degree of severity and management. We analysed the levels of the neutrophil-derived protein pro-LL-37 in plasma of patients with chronic neutropenia to assess whether it could be used to differentiate different categories of chronic neutropenia. All patients with severe congenital neutropenia were pro-LL-37 deficient. This was in contrast to patients with autoimmune or idiopathic neutropenia, who exhibited normal pro-LL-37 levels while patients with cyclic neutropenia displayed an oscillation of pro-LL-37 in plasma. Plasma levels of pro-LL-37 may thus prove useful for differential diagnosis of chronic neutropenia. 相似文献
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Hiroki Kurahashi Junichi Hara Keiko Yumura-Yag Akio Tawa Keisei Kawa-Ha 《Leukemia & lymphoma》1992,8(6):465-475
Recent data have elucidated the pathogenesis of transient abnormal myelopoiesis (TAM) to a great extent. TAM is a monoclonal disorder which resolves spontaneously and the target cell in this disorder is a multipotent stem cell which is capable of differentiating into megakaryocytes. The pathogeneses of TAM/AMKL (acute megakaryoblastic leukemia) appears to be closely associated with abnormal quality and quantity of a gene located on chromosome 21. AMKL developing after the regression of TAM appears to come from the same clone as the TAM, which apparently experiences some kind of genetic alterations. It seems that the gene responsible for TAM will soon be cloned in the near future. However, the mechanism of spontaneous regression of TAM has as yet not been clarified. The expanding clone in the transient phsysiological immunodeficient state, during the perinatal period, might be eliminated with the maturation of more mature immunosurveilance. Alternatively, the TAM clone might be destined to undergo spontaneous death, which is called “programmed cell death” (apoptosis). The mechanism of this phenomenon awaits further elucidation. 相似文献