Impaired induction of the CD28-responsive complex in granulocyte colony-stimulating factor mobilized CD4 T cells.

Publication Type:

Journal Article


Blood, Volume 91, Issue 1, p.347-52 (1998)


Adult, Antigens, CD, Antigens, CD14, Antigens, CD28, Antigens, CD80, Antigens, Differentiation, CD4-Positive T-Lymphocytes, CTLA-4 Antigen, DNA-Binding Proteins, Gene Expression Regulation, Granulocyte Colony-Stimulating Factor, Hematopoietic Stem Cell Mobilization, Humans, Immunoconjugates, Interleukin-2, Leukapheresis, Leukocytes, Mononuclear, Lymphocyte Activation, Lymphocyte Culture Test, Mixed, Muromonab-CD3, Promoter Regions, Genetic, Regulatory Sequences, Nucleic Acid, TRANSCRIPTION FACTORS, Transcription, Genetic


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.