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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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