Inhibition of human bone marrow and myeloid progenitors by interleukin 2-activated lymphocytes.
We have shown that unstimulated and interleukin 2 (IL-2)-activated peripheral blood lymphocytes from both normal donors and cancer patients in remission significantly inhibited the proliferation and granulocyte-macrophage colony formation (granulocyte-macrophage colony-forming cells, GM-CFC) of autologous and allogeneic bone marrow (BM). The inhibition was mediated primarily by CD5+ T cells, although lower levels of inhibition were also displayed by CD56+, CD5- lymphocytes, most of which were CD16-. The CD5+ lymphocytes were also the major effectors responsible for lysis of BM. Inhibition of BM proliferation and GM-CFC colony formation was not dependent on proliferation of the effector cells or cell-to-cell contact, because it was also mediated by a soluble factor produced by IL-2-activated lymphocytes. The relevance of these findings to future approaches to leukemia treatment is discussed.
Savary
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CA
Department of General Surgery, University of Texas, M.D. Anderson Cancer Center, Houston 77030.
Lotzová
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D015703:Antigens, CD / Q000032:analysis; D001853:Bone Marrow / Q000473:pathology*; D002455:Cell Division; D006098:Granulocytes / Q000473:pathology*; D006412:Hematopoietic Stem Cells / Q000473:pathology*; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology*; D015979:Killer Cells, Lymphokine-Activated / Q000502:physiology; D007694:Killer Cells, Natural / Q000502:physiology; D007938:Leukemia / Q000473:pathology; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000502:physiology*; D008264:Macrophages / Q000473:pathology; D009369:Neoplasms / Q000473:pathology*; D016176:T-Lymphocyte Subsets; D013601:T-Lymphocytes / Q000502:physiology
D015703:Antigens, CD; D007376:Interleukin-2