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Curr Opin Immunol. 2002 Feb;14(1):75-83.

Interactions between MHC molecules and co-receptors of the TCR.

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Department of Microbiology and Immunology and the Sealy Center for Molecular Science, The University of Texas Medical Branch, Galveston, TX 77555-1070, USA.


Genetic experiments indicate similarity between binding sites on MHC class I (MHCI) for CD8 and on MHCII for CD4, but the crystal structures of CD8/MHCI and CD4/MHCII complexes suggest critical differences between the interfaces in the two complexes. Biophysical analyses using ectodomains of co-receptors and MHC molecules demonstrate extremely fast kinetics and low-affinity interactions. Experiments with soluble multimeric MHC ligands suggest that CD4 and CD8 may differ in the mechanisms by which they promote the formation of ternary TCR/MHC/co-receptor complexes. Co-receptor-influenced duration of TCR signaling controls thymocyte selection. In naïve T cells, CD4/MHCII interactions may promote T-cell survival. Temporal and spatial analysis of TCR and CD4 co-clustering in the immunological synapse suggests that CD4 recruitment is regulated by the half-life of the initial TCR/MHCII complex. Diverse experimental systems have yielded conflicting data that have helped to formulate revised mechanistic models of co-receptor function.

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