Relationship of cell-cycle expression of ia-like antigenic determinants on normal and leukemia human granulocyte-macrophage progenitor cells to regulation in vitro by acidic isoferritins

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Abstract

An association has been established between human Ia-like (Ia) antigenic determinants, expression during DNA synthesis or granulocyte-macrophage colony forming cells (CFU-GM) and the regulatory action of acidic isoferritins in vitro. Treatment of human bone marrow cells with monoclonal-anti-Ia-like (Ia) plus complement inhibited colony and cluster formation by ~50% but did not affect pre-CFU-GM. Reduction of colonies and clusters was similar whether bone marrow cells were exposed to anti-Ia plus complement, high specific activity tritiated thymidine (3HTdr) or acidic isoferritins. No further decrease was apparent with 3HTdr or acidic isoferritins after Ia-antigen+ CFU-GM were removed, or with anti-Ia plus complement or acidic isoferritins after DNA synthetic phase (S-phase) CFU-GM were removed. Anti-Ia, without complement, did not reduce colony or cluster formation but did block the inhibitory action of acidic isoferritins. A relationship existed between Ia antigens and the activity of acidic isoferritins in the following ways: (a) The apparent loss of Ia-antigens from CFU-GM by 5 h in culture at 37°C, but not at 27° or 4°C, was associated with nonresponsiveness to inhibition with acidic isoferritins, (b) Ia-antigen-, noncycling pre-CFU-GM that were insensitive to acidic isoferritins could generate a population of Ia-antigen+ cycling CFU-GM in vitro that were responsive to inhibition by acidic isoferritins, and (c) nondetectability of Ia-antigens on CFU-GM from patients with leukemia was associated with nonresponsiveness to inhibition by acidic isoferritins. These results implicate Ia-antigen+ progenitor cells in the regulation of myelopoiesis in vitro and demonstrate that absence of Ia-antigens on patient CFU-GM is associated with imbalances in normal regulatory interactions in vitro. These findings may be of relevance to normal regulation and to the progression of leukemia.

Original languageEnglish (US)
Pages (from-to)632-642
Number of pages11
JournalJournal of Clinical Investigation
Volume69
Issue number3
StatePublished - 1982
Externally publishedYes

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Granulocyte-Macrophage Progenitor Cells
Histocompatibility Antigens Class II
Epitopes
Cell Cycle
Leukemia
Bone Marrow Cells
In Vitro Techniques
acidic isoferritin
Myelopoiesis
DNA
Granulocytes
Thymidine
Stem Cells
Macrophages

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{db9d6ff0c18a4357a17536d6580f289e,
title = "Relationship of cell-cycle expression of ia-like antigenic determinants on normal and leukemia human granulocyte-macrophage progenitor cells to regulation in vitro by acidic isoferritins",
abstract = "An association has been established between human Ia-like (Ia) antigenic determinants, expression during DNA synthesis or granulocyte-macrophage colony forming cells (CFU-GM) and the regulatory action of acidic isoferritins in vitro. Treatment of human bone marrow cells with monoclonal-anti-Ia-like (Ia) plus complement inhibited colony and cluster formation by ~50{\%} but did not affect pre-CFU-GM. Reduction of colonies and clusters was similar whether bone marrow cells were exposed to anti-Ia plus complement, high specific activity tritiated thymidine (3HTdr) or acidic isoferritins. No further decrease was apparent with 3HTdr or acidic isoferritins after Ia-antigen+ CFU-GM were removed, or with anti-Ia plus complement or acidic isoferritins after DNA synthetic phase (S-phase) CFU-GM were removed. Anti-Ia, without complement, did not reduce colony or cluster formation but did block the inhibitory action of acidic isoferritins. A relationship existed between Ia antigens and the activity of acidic isoferritins in the following ways: (a) The apparent loss of Ia-antigens from CFU-GM by 5 h in culture at 37°C, but not at 27° or 4°C, was associated with nonresponsiveness to inhibition with acidic isoferritins, (b) Ia-antigen-, noncycling pre-CFU-GM that were insensitive to acidic isoferritins could generate a population of Ia-antigen+ cycling CFU-GM in vitro that were responsive to inhibition by acidic isoferritins, and (c) nondetectability of Ia-antigens on CFU-GM from patients with leukemia was associated with nonresponsiveness to inhibition by acidic isoferritins. These results implicate Ia-antigen+ progenitor cells in the regulation of myelopoiesis in vitro and demonstrate that absence of Ia-antigens on patient CFU-GM is associated with imbalances in normal regulatory interactions in vitro. These findings may be of relevance to normal regulation and to the progression of leukemia.",
author = "Hal Broxmeyer",
year = "1982",
language = "English (US)",
volume = "69",
pages = "632--642",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "3",

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TY - JOUR

T1 - Relationship of cell-cycle expression of ia-like antigenic determinants on normal and leukemia human granulocyte-macrophage progenitor cells to regulation in vitro by acidic isoferritins

AU - Broxmeyer, Hal

PY - 1982

Y1 - 1982

N2 - An association has been established between human Ia-like (Ia) antigenic determinants, expression during DNA synthesis or granulocyte-macrophage colony forming cells (CFU-GM) and the regulatory action of acidic isoferritins in vitro. Treatment of human bone marrow cells with monoclonal-anti-Ia-like (Ia) plus complement inhibited colony and cluster formation by ~50% but did not affect pre-CFU-GM. Reduction of colonies and clusters was similar whether bone marrow cells were exposed to anti-Ia plus complement, high specific activity tritiated thymidine (3HTdr) or acidic isoferritins. No further decrease was apparent with 3HTdr or acidic isoferritins after Ia-antigen+ CFU-GM were removed, or with anti-Ia plus complement or acidic isoferritins after DNA synthetic phase (S-phase) CFU-GM were removed. Anti-Ia, without complement, did not reduce colony or cluster formation but did block the inhibitory action of acidic isoferritins. A relationship existed between Ia antigens and the activity of acidic isoferritins in the following ways: (a) The apparent loss of Ia-antigens from CFU-GM by 5 h in culture at 37°C, but not at 27° or 4°C, was associated with nonresponsiveness to inhibition with acidic isoferritins, (b) Ia-antigen-, noncycling pre-CFU-GM that were insensitive to acidic isoferritins could generate a population of Ia-antigen+ cycling CFU-GM in vitro that were responsive to inhibition by acidic isoferritins, and (c) nondetectability of Ia-antigens on CFU-GM from patients with leukemia was associated with nonresponsiveness to inhibition by acidic isoferritins. These results implicate Ia-antigen+ progenitor cells in the regulation of myelopoiesis in vitro and demonstrate that absence of Ia-antigens on patient CFU-GM is associated with imbalances in normal regulatory interactions in vitro. These findings may be of relevance to normal regulation and to the progression of leukemia.

AB - An association has been established between human Ia-like (Ia) antigenic determinants, expression during DNA synthesis or granulocyte-macrophage colony forming cells (CFU-GM) and the regulatory action of acidic isoferritins in vitro. Treatment of human bone marrow cells with monoclonal-anti-Ia-like (Ia) plus complement inhibited colony and cluster formation by ~50% but did not affect pre-CFU-GM. Reduction of colonies and clusters was similar whether bone marrow cells were exposed to anti-Ia plus complement, high specific activity tritiated thymidine (3HTdr) or acidic isoferritins. No further decrease was apparent with 3HTdr or acidic isoferritins after Ia-antigen+ CFU-GM were removed, or with anti-Ia plus complement or acidic isoferritins after DNA synthetic phase (S-phase) CFU-GM were removed. Anti-Ia, without complement, did not reduce colony or cluster formation but did block the inhibitory action of acidic isoferritins. A relationship existed between Ia antigens and the activity of acidic isoferritins in the following ways: (a) The apparent loss of Ia-antigens from CFU-GM by 5 h in culture at 37°C, but not at 27° or 4°C, was associated with nonresponsiveness to inhibition with acidic isoferritins, (b) Ia-antigen-, noncycling pre-CFU-GM that were insensitive to acidic isoferritins could generate a population of Ia-antigen+ cycling CFU-GM in vitro that were responsive to inhibition by acidic isoferritins, and (c) nondetectability of Ia-antigens on CFU-GM from patients with leukemia was associated with nonresponsiveness to inhibition by acidic isoferritins. These results implicate Ia-antigen+ progenitor cells in the regulation of myelopoiesis in vitro and demonstrate that absence of Ia-antigens on patient CFU-GM is associated with imbalances in normal regulatory interactions in vitro. These findings may be of relevance to normal regulation and to the progression of leukemia.

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