Suppressive effects of recombinant human monokine induced by IFN-gamma (rHuMig) chemokine on the number of committed and primitive hemopoietic progenitors in liquid cultures of CD34+ human bone marrow cells.

Studies in this report investigated potential hemopoietic suppressive effects of human monokine induced by IFN-gamma (HuMig), a CXC chemokine that is chemotactic for activated lymphocytes. rHuMig was purified from Trichoplusia ni cells after infection with a recombinant baculovirus. The recombinant protein was added to liquid cultures of CD34+ human marrow cells stimulated with IL-3 alone or with both IL-3 and either insulin-like growth factor II (IGF-II) or stem cell growth factor (SCF). The number of committed progenitors, colony-forming units for granulocytes and macrophages (CFU-GM), and primitive progenitors, long term culture-initiating cells (LTC-IC) derived from liquid cultures of CD34+ cells, was determined. rHuMig abrogated the IGF-II-dependent enhancement of CFU-GM and long term culture-initiating cell numbers. Additional studies demonstrated that in liquid cultures of CD34+ cells both rHuMig and IFN-inducible protein-10, another CXC chemokine that is related to HuMig, inhibited the production or expansion of CFU-GM. For a subset of marrows, rHuMig also abrogated SCF enhancement of CFU-GM numbers in cultures of CD34+ cells stimulated with both IL-3 and SCF. These studies are the first to demonstrate that rHuMig can act as a negative regulator of in vitro hemopoiesis, that both rHuMig and IP-10 can suppress an increase in the number of committed progenitors from CD34+ cells, and that chemokines can abrogate hemopoietic stimulatory effects of IGF-II.

• Publication year

  1997

• Venue

  Journal of Immunology

• Publication date

  1997-07-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.4049/jimmunol.159.2.895PMID 9218609
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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