Ligation of MHC class I molecules on peripheral blood T lymphocytes induces new phenotypes and functions
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Ligation of MHC class I molecules on peripheral blood T lymphocytes induces new phenotypes and functions. / Bregenholt, S; Röpke, M; Skov, S; Claesson, Mogens Helweg.
In: Journal of Immunology, Vol. 157, No. 3, 01.08.1996, p. 993-9.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Ligation of MHC class I molecules on peripheral blood T lymphocytes induces new phenotypes and functions
AU - Bregenholt, S
AU - Röpke, M
AU - Skov, S
AU - Claesson, Mogens Helweg
PY - 1996/8/1
Y1 - 1996/8/1
N2 - 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.
AB - 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.
KW - Antibodies, Monoclonal
KW - Antigens, CD28
KW - Antigens, CD3
KW - Cell Division
KW - Cytotoxicity, Immunologic
KW - Dose-Response Relationship, Immunologic
KW - Histocompatibility Antigens Class I
KW - Humans
KW - Phenotype
KW - Phosphorylation
KW - Protein-Tyrosine Kinases
KW - Receptors, Antigen, T-Cell
KW - T-Lymphocyte Subsets
KW - Time Factors
M3 - Journal article
C2 - 8757602
VL - 157
SP - 993
EP - 999
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 3
ER -
ID: 227123