Abnormalities in Myelopoietic Regulatory Interactions With Acidic Isoferritins and Lactoferrin in Mice Infected With Friend Virus Complex: Association With Altered Expression of Ia Antigens on Effector and Responding Cells

The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells. Under normal conditions, AIF suppresses col...

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Bibliographic Details
Published in:	Blood Vol. 65; no. 1; pp. 91 - 99
Main Authors:	Lu, Li, Broxmeyer, Hal E., Moore, Malcolm A.S., Sheridan, Alice P., Gentile, Patrick
Format:	Journal Article
Language:	English
Published:	Washington, DC Elsevier Inc 01-01-1985 The Americain Society of Hematology
Subjects:	Animal tumors. Experimental tumors Animals Biological and medical sciences Colony-Stimulating Factors - antagonists & inhibitors Drug Interactions Experimental malignant blood diseases Female Ferritins - metabolism Ferritins - pharmacology Friend murine leukemia virus Hematopoiesis - drug effects Hematopoietic Stem Cells - immunology Hematopoietic Stem Cells - pathology Histocompatibility Antigens Class II - analysis Lactoferrin - metabolism Lactoferrin - pharmacology Lactoglobulins - pharmacology Leukemia, Experimental - immunology Leukemia, Experimental - pathology Lipoproteins - pharmacology Medical sciences Mice Mice, Inbred BALB C Moloney murine leukemia virus Proteins Tumors Hematopoietic cell Molecular interaction Iron Ia-System Lactoferrin Regulation(control) CFU-GM-Cell Friend leukemia Target cell Myelopoiesis Carrier protein Oncovirinae Histocompatibility system Hematology Rodentia Retroviridae Malignant hemopathy Experimental animal Gene expression Infection Virus Vertebrata Mammalia Alloantigen Mouse Type C oncovirus Viral disease Murine leukemia virus Experimental tumor Granulocyte macrophage colony stimulating activity
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Summary:	The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells. Under normal conditions, AIF suppresses colony and cluster formation by an la-antigen-positive cycling subpopulation of mouse granulocyte-macrophage progenitor cells (CFU-GM). Under the same conditions, the release of AlF-inhibitory activity and granulocyte-macrophage colony stimulatory factors (GM-CSF) from an la-antigen-positive subpopulation of monocytes and macrophages is suppressed by LF. Within one to two days after inoculation in vivo with Friend virus complex or helper virus, mouse CFU-GM become insensitive in vitro to suppression by purified human AIF as well as crude mouse AIF, and by four days, bone marrow, spleen, and thymus cells of these mice release much greater quantities of AlF-inhibitory activity than the cells from mice injected with control medium. The Friend virus complex itself has no influence in vitro on CFU-GM from normal mice. In addition, the release of AlF-inhibitory activity from bone marrow, spleen, and resident peritoneal cells and the release of GM-CSF from resident peritoneal cells of mice infected with Friend virus complex are not suppressed by LF. The inability of AIF to suppress colony formation by bone marrow and spleen CFU-GM from mice infected with Friend virus complex is associated with the loss of Ia (I-A subregion) antigens from CFU-GM, even though CFU-GM are in cycle. The nonresponsiveness of bone marrow, spleen, and peritoneal cells from these mice to LF suppression of AIF release and the inability of LF to influence GM-CSF release from peritoneal cells is associated with loss of Ia antigens from these cells. The above abnormalities are similar to the defects noted using cells from patients with leukemia. These results suggest that mice infected with Friend virus complex can serve as a model for investigating abnormalities in cell regulation and their relationships to disease progression.
ISSN:	0006-4971 1528-0020
DOI:	10.1182/blood.V65.1.91.91