title: T-cell regulation of erythropoiesis during acute lymphoblastic leukemia.
abstract: How and where erythropoiesis is maintained during advanced leukemic disease is an important and, as yet, unresolved question in hematology. To address the potential role of T-lymphocytes as cells that regulate CFU-E differentiation during leukemogenesis, an experimental model of disease has been developed in inbred Balb/c mice. Specifically, three-week-old Balb/c By mice were injected with murine sarcoma virus-murine leukemia virus-Moloney (MSV-MuLV-M), which resulted 6-8 months later in the development of immunoblastic T-cell sarcomas with a leukemic phase. Splenic T cells from either normal or tumor-bearing mice were assessed for their relative ability to modulate erythroid differentiation. Quantitatively, T cells, Ly1 or Ly 2,3 T-cell subsets isolated from tumor-bearing animals significantly enhanced erythropoiesis when compared with comparable normal T-cell subsets. These data suggest that the compensatory shift of erythropoiesis from the bone marrow to the spleen observed during leukemogenesis was facilitated by splenic T cells. In this circumstance, the enhanced erythropoietic function may be mediated by splenic T cells, which are selectively activated by virus.
mesh_terms: D000818:Animals; D000950:Antigens, Ly / Q000032:analysis; D000951:Antigens, Neoplasm / Q000032:analysis; D001853:Bone Marrow / Q000473:pathology; D004920:Erythropoiesis; D005260:Female; D007942:Leukemia, Experimental / Q000503:physiopathology*; D007945:Leukemia, Lymphoid / Q000503:physiopathology*; D008223:Lymphoma / Q000503:physiopathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008979:Moloney murine leukemia virus; D008980:Moloney murine sarcoma virus; D013154:Spleen / Q000473:pathology; D013601:T-Lymphocytes / Q000502:physiology*
chemical_list: D000950:Antigens, Ly; D000951:Antigens, Neoplasm