T-cell regulation of erythropoiesis during acute lymphoblastic leukemia.
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.
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*
D000950:Antigens, Ly; D000951:Antigens, Neoplasm