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International Immunology, Vol. 11, No. 11, 1745-1752, November 1999
© 1999 Japanese Society for Immunology

The MHC class II ligand lymphocyte activation gene-3 is co-distributed with CD8 and CD3–TCR molecules after their engagement by mAb or peptide–MHC class I complexes

Sigrid Hannier and Frédéric Triebel

Laboratoire d'Immunologie Cellulaire, Institut Gustave-Roussy, 39, rue Camille Desmoulins, 94805 Villejuif and Laboratoire d'Immunologie des tumeurs, Faculté de Pharmacie, Université Paris XI, 5 rue Jean-Baptiste Clément, 92296 Chatenay-Malabry, France

Correspondence to: F. Triebel, Institut Gustave-Roussy, 39 rue Camille Desmoulins, 94805 Villejuif, France

Previous studies indicated that signaling through lymphocyte activation gene-3 (LAG-3), a MHC class II ligand, induced by multivalent anti-receptor antibodies led to unresponsiveness to TCR stimulation. Here, lateral distribution of the LAG-3 molecules and its topological relationship (mutual proximity) to the TCR, CD8, CD4, and MHC class I and II molecules were studied in the plasma membrane of activated human T cells in co-capping experiments and conventional fluorescence microscopy. Following TCR engagement by either TCR-specific mAb or MHC–peptide complex recognition in T–B cell conjugates, LAG-3 was found to be specifically associated with the CD3–TCR complex. Similarly, following CD8 engagement LAG-3 and CD8 were co-distributed on the cell surface while only a low percentage of CD4-capped cells displayed LAG-3 co-caps. In addition, LAG-3 was found to be associated with MHC class II (i.e. DR, DP and DQ) and partially with MHC class I molecules. The supramolecular assemblies described here between LAG-3, CD3, CD8 and MHC class II molecules may result from an organization in raft microdomains, a phenomenon known to regulate early events of T cell activation.

Keywords: MHC, T cell, TCR

Transmitting editor: A. McMichael


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