These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Lack of normal CFU-C/suppressor activity in population of alloantigen-stimulated T cells from patients with chronic myelogenous leukemia.
    Author: Maekawa T, Sonoda Y, Yokota S, Abe T.
    Journal: Exp Hematol; 1986 May; 14(4):316-23. PubMed ID: 2938981.
    Abstract:
    Alloantigen-stimulated T cells from patients with Ph1-positive chronic myelogenous leukemia (CML) and normal individuals were obtained by one-way mixed lymphocyte cultures (MLC). Effects of alloantigen-stimulated T cells and MLC supernatants on colony formation were studied in vitro. Alloantigen-stimulated T cells were cocultured with normal allogeneic bone marrow cells (target cells) grown for CFU-C and BFU-E formation. Target cells were also cultured with MLC supernatants. Alloantigen-stimulated T cells from normal controls significantly suppressed CFU-C formation in the presence of human placental conditioned medium (HPCM), while those from CML patients failed to reduce it. MLC supernatants from CML patients were significantly less suppressive on CFU-C formation than those from normal controls. In contrast, not only normal and CML alloantigen-stimulated T cells but also their MLC supernatants increased BFU-E formation in a similar manner. Furthermore, MLC supernatants from normal controls as well as CML patients stimulated the growth of CFU-C from target cells in the absence of HPCM. These results suggest that CML T cells lack the ability to release soluble inhibitors of granulopoiesis, although the production of colony-stimulating factors and burst-promoting activities was equivalent to that of normal T cells after alloantigen stimulation in vitro. The failure of CML T cells to suppress granulopoiesis may contribute to the preferential proliferation of granulocytes in the pathophysiology of CML.
    [Abstract] [Full Text] [Related] [New Search]