Expression of Ia-antigens on normal and chronic myeloid leukemic human granulocyte-macrophage colony-forming cells (CFU-GM) is associated with the regulation of cell proliferation by prostaglandin E

L. M. Pelus, S. Saletan, R. T. Silver, M. A.S. Moore

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

The presence of Ia-antigens and their relationship to the inhibitory effect of prostaglandin E on the proliferation of human CFU-GM was studied in normals and patients with chronic myeloid leukemia. Consistent reduction of normal colony formation to approximately 50% of baseline levels was observed using a monoclonal anti-human Ia antibody in a complement-dependent cytotoxicity assay titrated over serial dilutions. Elimination of the Ia-antigen-bearing CFU-GM population was associated with virtually a complete loss of responsiveness to the inhibitory effects of prostaglandin E. Maintenance of bone marrow cells in short-term suspension culture at 37°C prior to agar culture resulted in the loss of detectable Ia-antigen on the CFU-GM and, similarly, loss of response to prostaglandin. In contrast, most patients with chronic myeloid leukemia showed greatly reduced levels of Ia-antigens on their CFU-GM in fresh marrow together with lack of prostaglandin sensitivity, suggesting a correlation with the abnormal growth regulation observed in these patients. In two chronic myeloid leukemia patients, levels of Ia-antigen higher than that observed in the majority of patients could be detected and correlated with a residual response to prostaglandin E. These results suggst a relationship in normals between the expression of Ia-antigens on CFU-GM and the physiologic response to regulation by prostaglandin E, and a possible mechanism for the aberrant regulatory response in patients with chronic myeloid leukemia.

Original languageEnglish (US)
Pages (from-to)284-292
Number of pages9
JournalBlood
Volume59
Issue number2
DOIs
StatePublished - 1982

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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