Abstract
Microgram concentrations of immobilized anti-MHC class I (MHC-I) Ab induced proliferation of resting CD3+ T cells from peripheral blood. In contrast, soluble Ab did not activate T cells. Exposure of T cells to immobilized anti-MHC-I Ab for only 24 h was followed by proliferation and development of T cell-mediated cytotoxicity. Immediately following MHC-I ligation, the T cells responded with increased protein tyrosine phosphorylation, with new bands appearing in the SDS-PAGE. Exposure of T cells to immobilized anti-MHC-I Ab for 24 h induced an increased surface expression of the TCR/CD3 and CD28 molecules. MHC-I-induced proliferation of purified T cells was dependent on cellular interactions with non-T cells. Under certain conditions, in which MHC-I was ligated by picogram concentrations of immobilized anti-MHC-I Ab, anti-TCR/CD3 Ab-induced proliferation of T cells was strongly inhibited. These data clearly demonstrate that ligation of the MHC-I complex on T cells may induce both positive and negative signals. Since the physiologic ligands for MHC-I molecules are TCR and the CD8 molecules, our data may suggest that MHC-I molecules are instrumental in cellular interactions between T cells.
Original language | English |
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Journal | Journal of Immunology |
Volume | 157 |
Issue number | 3 |
Pages (from-to) | 993-9 |
Number of pages | 7 |
ISSN | 0022-1767 |
Publication status | Published - 1 Aug 1996 |
Keywords
- Antibodies, Monoclonal
- Antigens, CD28
- Antigens, CD3
- Cell Division
- Cytotoxicity, Immunologic
- Dose-Response Relationship, Immunologic
- Histocompatibility Antigens Class I
- Humans
- Phenotype
- Phosphorylation
- Protein-Tyrosine Kinases
- Receptors, Antigen, T-Cell
- T-Lymphocyte Subsets
- Time Factors