title: Interaction of monocytes and T cells in the regulation of normal human megakaryocytopoiesis in vitro: role of IL-1 and IL-2.
abstract: Autologous or allogeneic peripheral blood T cells can stimulate the human megakaryocyte progenitor cell (CFU-Meg)-derived colony formation in a dose-dependent fashion in agar cultures of nonadherent (NA), T cell-depleted (NT) bone marrow (BM) cells. Low concentrations of monocytes and T cells can collaborate in the stimulation of CFU-Meg colony formation or in the production of megakaryocyte colony stimulating factor (Meg-CSF) by T cells in the presence of mitogens or IL-2. Monocytes alone can produce only negligible Meg-CSF under any conditions. When monocyte conditioned medium (CM) was added to T cell-stimulated NA, NT BM cell cultures, CFU-Meg colony growth was appreciably increased compared with that stimulated by T cells alone. Dose-dependent increase in CFU-Meg colony growth was noted when varying concentrations of IL-1 were added to T cell-stimulated NA, NT cell cultures, although IL-1 itself could support no CFU-Meg colony growth in the absence of T cells. These data suggest that a synergistic interaction between T cells and monocytes during the production of Meg-CSF by T cells could be partly mediated by IL-1. IL-2 was found to stimulate Meg-CSF production by T cells in the presence or absence of mitogens. IL-2-stimulated Meg-CSF production by T cells was augmented by the addition of monocytes. Although IL-2 itself had no stimulatory effect on CFU-Meg colony growth, dramatic augmentation in the CFU-Meg colony number was noted when IL-2 was added to T cell-stimulated NA, NT cell cultures. High concentrations of monocytes and prostaglandin E (PGE) inhibited the CFU-Meg colony formation. These results suggest that IL-1 and IL-2 may play a stimulatory role on the normal human in vitro megakaryocytopoiesis, and may be involved in the development of reactive thrombocytosis and bone marrow megakaryocytic hyperplasia in various inflammatory diseases.
authors.affiliation: Department of Internal Medicine, Musashino Red Cross Hospital, Tokyo, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Hamaguchi
authors.forename: N
authors.initials: N
authors.lastname: Takano
authors.forename: K
authors.initials: K
authors.lastname: Saito
authors.forename: H
authors.initials: H
authors.lastname: Enokihara
authors.forename: S
authors.initials: S
authors.lastname: Furusawa
authors.forename: H
authors.initials: H
authors.lastname: Shishido
mesh_terms: D002450:Cell Communication / Q000502:physiology; D002478:Cells, Cultured; D002999:Clone Cells / Q000166:cytology; D003114:Colony-Forming Units Assay; D058851:GPI-Linked Proteins; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology*; D007376:Interleukin-2 / Q000502:physiology*; D008533:Megakaryocytes / Q000166:cytology*; D008562:Membrane Glycoproteins; D000090204:Mesothelin; D009000:Monocytes / Q000502:physiology*; D014176:Protein Biosynthesis; D011506:Proteins; D011994:Recombinant Proteins / Q000502:physiology; D013601:T-Lymphocytes / Q000502:physiology*
chemical_list: D058851:GPI-Linked Proteins; D007375:Interleukin-1; D007376:Interleukin-2; D008562:Membrane Glycoproteins; D011506:Proteins; D011994:Recombinant Proteins; D000090204:Mesothelin