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Prepublished online as a Blood First Edition Paper on April 3, 2003; DOI 10.1182/blood-2002-04-1200.
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Blood, 15 July 2003, Vol. 102, No. 2, pp. 734-739
TRANSPLANTATION
G-CSF as immune regulator in T cells expressing the G-CSF receptor: implications for transplantation and autoimmune diseases
Anke Franzke,
Wenji Piao,
Jörg Lauber,
Patricia Gatzlaff,
Christian Könecke,
Wiebke Hansen,
Angela Schmitt-Thomsen,
Bernd Hertenstein,
Jan Buer, and
Arnold Ganser
From the Department of Hematology and Oncology, the Department of Transfusion Medicine, and the Institute of Medical Microbiology, Hannover Medical School, Hannover, Germany; and the Mucosal Immunity Group, GBF-Braunschweig, Braunschweig, Germany
Results from experimental models, in vitro studies, and clinical data indicate that granulocyte colony-stimulating factor (G-CSF) stimulation alters T-cell function and induces Th2 immune responses. The immune modulatory effect of G-CSF on T cells results in an unexpected low incidence of acute graft-versus-host disease in peripheral stem cell transplantation. However, the underlying mechanism for the reduced reactivity and/or alloreactivity of T cells upon G-CSF treatment is still unknown. In contrast to the general belief that G-CSF acts exclusively on T cells via monocytes and dendritic cells, our results clearly show the expression of the G-CSF receptor in class I– and II– restricted T cells at the single-cell level both in vivo and in vitro. Kinetic studies demonstrate the induction and functional activity of the G-CSF receptor in T cells upon G-CSF exposure. Expression profiling of T cells from G-CSF–treated stem cell donors allowed identification of several immune modulatory genes, which are regulated upon G-CSF administration in vivo (eg, LFA1- , ISGF3- ) and that are likely responsible for the reduced reactivity and/or alloreactivity. Most importantly, the induction of GATA-3, the master transcription factor for a Th2 immune response, could be demonstrated in T cells upon G-CSF treatment in vivo accompanied by an increase of spontaneous interleukin-4 secretion. Hence, G-CSF is a strong immune regulator of T cells and a promising therapeutic tool in acute graft-versus-host disease as well as in conditions associated with Th1/Th2 imbalance, such as bone marrow failure syndromes and autoimmune diseases.
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