Abstract
Abstract We here demonstrate that ligand binding to MHC class I molecules induces homotypic cell adhesion of lymphocytes and monocytes. mAb to beta 2-microglobulin caused sustained, largely LFA-1-independent adhesion whereas mAb to the MHC class I alpha H chain caused transient LFA-1-dependent adhesion. Both the protein kinase C inhibitor sphingosine and the tyrosine kinase inhibitor genistein abrogated MHC class I-mediated cellular adhesion. These results indicate that MHC class I molecules transduce signals that induce cell adhesion and suggest that interaction between MHC class I-restricted T cells and APC may result in reciprocal enhanced adhesiveness of these cells.
Dates
Type | When |
---|---|
Created | 2 years, 8 months ago (Dec. 31, 2022, 4:59 a.m.) |
Deposited | 7 months, 4 weeks ago (Jan. 2, 2025, 11:30 a.m.) |
Indexed | 2 months ago (June 27, 2025, 9:46 a.m.) |
Issued | 33 years, 5 months ago (April 1, 1992) |
Published | 33 years, 5 months ago (April 1, 1992) |
Published Print | 33 years, 5 months ago (April 1, 1992) |
@article{Spertini_1992, title={Engagement of MHC class I molecules induces cell adhesion via both LFA-1-dependent and LFA-1-independent pathways.}, volume={148}, ISSN={1550-6606}, url={http://dx.doi.org/10.4049/jimmunol.148.7.2045}, DOI={10.4049/jimmunol.148.7.2045}, number={7}, journal={The Journal of Immunology}, publisher={Oxford University Press (OUP)}, author={Spertini, F and Chatila, T and Geha, R S}, year={1992}, month=apr, pages={2045–2049} }