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Impaired Induction of the CD28-Responsive Complex in Granulocyte Colony-Stimulating Factor Mobilized CD4 T Cells

Junji Tanaka, Marco Mielcarek, and Beverly Torok-Storb

From the Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA and the Department of Medicine, University of Washington, Seattle, WA.

Use of the CD28/B7 costimulatory signal for T-cell activation was analyzed in granulocyte colony-stimulating factor (G-CSF) mobilized peripheral blood mononuclear cells (G-PBMCs) and in peripheral blood mononuclear cells obtained before administration of G-CSF (preG-PBMCs). CTLA4Ig inhibition of OKT3-stimulated proliferation was significantly lower in G-PBMCs compared with preG-PBMCs (39.9% ± 5.6% and 72.2% ± 5.4%, respectively; P < .001). Furthermore, as shown in electrophoretic mobility-shift assays, the inducible level of the T-cell transcription factor CD28 responsive complex (CD28RC) was suppressed in CD4 cells derived from G-PBMC. However, depletion of CD14 cells from G-PBMCs restored CD28RC induction to normal levels. Taken together, these findings suggest that the large number of CD14 monocytes in G-PBMCs may limit T-cell responsiveness by suppressing the induction of the CD28RC.

Blood, Vol. 91 No. 1 (January 1), 1998: pp. 347-352
© 1998 by The American Society of Hematology.


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