Comparative analysis of the human macrophage inflammatory protein family of cytokines (chemokines) on proliferation of human myeloid progenitor cells. Interacting effects involving suppression, synergistic suppression, and blocking of suppression.

摘要: Macrophage inflammatory protein (MIP)-1 alpha, part of a family termed chemokines, has been implicated in suppression hemopoietic stem and progenitor cell proliferation. The chemokine organized into two subgroups with MIP-1 beta, macrophage chemotactic activating factor (MCAF) RANTES belonging to one subgroup, GRO-alpha, MIP-2 alpha (GRO-beta), beta (GRO-gamma), platelet 4 (PF4), IL-8, neutrophil peptide (NAP)-2 the other. These molecules were evaluated for effects on colony formation by human bone marrow multipotential (CFU-GEMM), erythroid (BFU-E) granulocyte-macrophage (CFU-GM) cells. None chemokines stimulated absence CSF, or influenced single growth such as granulocyte-macrophage-CSF erythropoietin. However, PF4, MCAF suppressed dose-response fashion immature subsets myeloid cells GM-CSF plus steel factor. Effects apparent low density CD34 HLA-DR(+)-sorted which up 88.4% composed cells, suggesting direct progenitors themselves. Up 2500-fold less each could be used demonstrate synergistic when any these five together at concentrations, also apparently directly progenitors. In contrast, NAP-2, not suppressive nor did they synergize suppress. fivefold excess blocked alpha. Similarly, either GRO-alpha IL-8 PF4. suppressing, synergizing blocking may relevance blood regulation.