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Release of granulocyte‐macrophage colony‐inhibiting activity by normal human postthymic precursor cells
Author(s) -
LópezKarpovitch X.,
PadrósSemorile M. R.,
Rojas R.,
MartínezSánchez L.
Publication year - 1985
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830200306
Subject(s) - lymphocyte , biology , buffy coat , macrophage , peripheral blood mononuclear cell , granulocyte , microbiology and biotechnology , immunology , granulocyte macrophage colony stimulating factor , cytokine , in vitro , biochemistry
Seven normal human peripheral blood cell fractions (buffy coat, mononuclear cells, non‐T, T, Fc‐IgM receptor‐depleted T‐lymphocyte, Fc‐IgG receptor‐depleted T‐lymphocyte, and autologous rosette‐forming T‐cell‐depleted T‐lymphocyte subpopulations) treated with phytohemagglutinin (PHA) were examined for the production of granulocyte‐macrophage colony‐stimulating activity (CSA). It was found that medium conditioned by a T‐lymphocyte subpopulation depleted of autologous rosette‐forming T‐cells (Tar cells, a postthymic precursor subpopulation that inhibits Ig synthesis) stimulated colony‐forming units of granulocyte and macrophages (CFU‐GM) to a greater extent than did the other conditioned media (CM) analyzed. Based on this finding, CM from an enriched Tar subpopulation was prepared and thus showed that PHA‐treated Tar cells release a factor capable of inhibiting CFU‐GM growth. The inhibitory activity of this factor persisted after heat inactivation, suggesting that cause of the colony‐inhibiting activity (CIA) is other than interferon. Further studies revealed that Tar‐derived inhibitory factor acts either directly upon CFU‐GM or via monocytes/macrophages (Mϕ/Ma), enhancing CIA, and not the level of CSA production by Mϕ/Ma. The overall data are interpreted as demonstrating the presence of CIA in a specific T‐lymphocyte subpopulation that may represent a new relationship between lymphocytic and myelocytic systems in the human.