Advertisement
Research Article Free access | 10.1172/JCI114016
Department of Hematology, University of Mainz, Federal Republic of Germany.
Find articles by Lindemann, A. in: JCI | PubMed | Google Scholar
Department of Hematology, University of Mainz, Federal Republic of Germany.
Find articles by Riedel, D. in: JCI | PubMed | Google Scholar
Department of Hematology, University of Mainz, Federal Republic of Germany.
Find articles by Oster, W. in: JCI | PubMed | Google Scholar
Department of Hematology, University of Mainz, Federal Republic of Germany.
Find articles by Ziegler-Heitbrock, H. in: JCI | PubMed | Google Scholar
Department of Hematology, University of Mainz, Federal Republic of Germany.
Find articles by Mertelsmann, R. in: JCI | PubMed | Google Scholar
Department of Hematology, University of Mainz, Federal Republic of Germany.
Find articles by Herrmann, F. in: JCI | PubMed | Google Scholar
Published April 1, 1989 - More info
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known as an inducer of proliferation and functional activation of myeloid cells. This study was carried out to characterize the effects of GM-CSF on polymorphonuclear leukocytes (PMN) more extensively. Using Northern blot analysis, we show that PMN are able to accumulate mRNAs for different cytokines, including tumor necrosis factor-alpha (TNF-alpha); G-CSF, and M-CSF, all of which are involved in inflammation and hematopoiesis. Biological assays and immunoassays demonstrate that PMN translate these mRNAs, except TNF-alpha, into secretory proteins. However, the expression of these cytokines is dependent on stimulation by exogenous signals, preferentially provided by the T cell-derived lymphokine GM-CSF. Stimulation of hematopoiesis and amplification of defense mechanisms after T cell activation thus might involve not only monocytes but also PMN, a cell type previously believed to be biosynthetically inactive.
Images.