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Published online before print January 23, 2004
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* Department of Immunology and Cell Biology, Research Center Borstel, Germany;
Centre for Molecular Neurobiology Hamburg, University Hospital Hamburg, Germany; and
Clinic for Surgery, University Hospital Lübeck, Germany
1Correspondence: Department of Immunology and Cell Biology, Research Center Borstel, Parkallee 22, D-23845 Borstel, Germany. E-mail: ajulmer@fz-borstel.de
Lipopolysaccharide (LPS) has been shown to induce proliferation of human T-lymphocytes only in the presence of monocytes and CD34+ hematopoietic cells (HCs) from peripheral blood. This finding provided evidence of an active role of CD34+ HCs during inflammation and immunological events. To investigate mechanisms by which CD34+ HCs become activated and exert their immune-modulatory function, we used the human CD34+ acute myeloid leukemia cell line KG-1a and CD34+ bone marrow cells (BMCs). We showed that culture supernatants of LPS-stimulated mononuclear cells (SUPLPS) as well as tumor necrosis factor 
(TNF-), but not LPS alone, can activate nuclear factor-
B in KG-1a cells. By cDNA subtraction and multiplex polymerase chain reaction, we revealed differential expression of cellular inhibitor of apoptosis protein-1, inhibitor of B (IB)/IB (MAD-3), and intercellular adhesion molecule-1 (ICAM-1) in SUPLPS-stimulated KG-1a cells and up-regulation of interferon (IFN)-inducible T cell-chemoattractant, interleukin (IL)-8, macrophage-inflammatory protein-1 (MIP-1), MIP-1ß, RANTES, CD70, granulocyte macrophage-colony stimulating factor, and IL-1ß in stimulated KG-1a cells and CD34+ BMCs. Although monokine induced by IFN-
, IFN-inducible protein 10, and IFN- were exclusively up-regulated in KG-1a cells, differential expression of monocyte chemoattractant protein-1 (MCP-1), macrophage-derived chemokine, myeloid progenitor inhibitory factor-2, and IL-18 receptor was only detectable in CD34+ BMCs. More importantly, CD34+ BMCs stimulated by TNF- also showed enhanced secretion of MCP-1, MIP-1, MIP-1ß, and IL-8, and increased ICAM-1 protein expression could be detected in stimulated KG-1a cells and CD34+ BMCs. Furthermore, we revealed that T cell proliferation can be induced by TNF--stimulated KG-1a cells, which is preventable by blocking anti-ICAM-1 monoclonal antibodies. Our results demonstrate that CD34+ HCs have the potential to express a variety of immune-regulatory mediators upon stimulation by inflammatory cytokines including TNF-, which may contribute to innate- and adaptive-immune processes.
Key Words: innate-immune modulation • T cell activation
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