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To initiate an immune response, key receptor-ligand pairs must cluster in "immune synapses" at the T cell-antigen-presenting cell (APC) interface. We visualized the accumulation of a major histocompatibility complex (MHC) class II molecule, I-E(k), at a T cell-B cell interface and found it was dependent on both antigen recognition and costimulation. This suggests that costimulation-driven active transport of T cell surface molecules helps to drive immunological synapse formation. Although only agonist peptide-MHC class II (agonist pMHC class II) complexes can initiate T cell activation, endogenous pMHC class II complexes also appeared to accumulate. To test this directly, we labeled a "null" pMHC class II complex and found that, although it lacked major TCR contact residues, it could be driven into the synapse in a TCR-dependent manner. Thus, low-affinity ligands can contribute to synapse formation and T cell signaling.

Original publication

DOI

10.1038/ni741

Type

Journal article

Journal

Nature immunology

Publication Date

01/2002

Volume

3

Pages

42 - 47

Addresses

The Howard Hughes Medical Institute and The Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Keywords

B-Lymphocytes, Cells, Cultured, Animals, Mice, Macromolecular Substances, Peptide Fragments, Lymphocyte Function-Associated Antigen-1, Luminescent Proteins, Green Fluorescent Proteins, Membrane Proteins, Receptors, Antigen, T-Cell, Antigens, CD28, Recombinant Fusion Proteins, Histocompatibility Antigens Class II, Autoantigens, Isoantigens, Ligands, Imaging, Three-Dimensional, Microscopy, Fluorescence, Microscopy, Video, Transfection, Lymphocyte Activation, Cell Communication, Cell Polarity, Immunologic Capping, Calcium Signaling, Self Tolerance, Genes, MHC Class II, Protein Transport, Genes, Reporter, Models, Immunological