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Updated: Aug 12, 2026

Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
Published on: June 13, 2014
Engagement of MHC class I molecules induces cell adhesion via both LFA-1-dependent and LFA-1-independent pathways
F Spertini1, T Chatila, R S Geha
1Division of Immunology, Children's Hospital, Boston, MA 02115.
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.
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.
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