Nature Immunology 3, 27 - 32 (2002)
DOI:10.1038/ni742
http://www.nature.com/nilink/v3/n1/abs/ni742_fs.html

在體內(nèi)T 細(xì)胞下調(diào)APC細(xì)胞表面MHC-肽類復(fù)合體

R M Kedl, B C Schaefer, J W Kappler & P Marrack
1 Department of Immunology, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, CO 80206, USA.
2 Department of Medicine, Howard Hughes Medical Institute, University of Colorado Health Sciences Center, Denver, CO 80206, USA.
3 Department of Pharmacology, University of Colorado Health Sciences Center, Denver, CO 80206, USA.
4 Department of Biochemistry and Molecular Genetics, University of Colorado Health Sciences Center, Denver, CO 80206, USA.
5 Present address: 3M Pharmaceuticals, 3M Center, Bldg. 270-02-S-06, St. Paul, MN 55144, USA.

T cells compete in the response to antigen in vivo and this competition may drive the affinity maturation of a secondary T cell response. Here we show that high-affinity T cells out-competed lower affinity T cells during a response to antigenic challenge in vivo. Although competition between T cells specific for different peptide–major histocompatibility complexes (MHC) occurred, it was less efficient than competition between T cells of the same peptide-MHC specificity. In addition, high-affinity T cells efficiently induced antigen loss from the surface of antigen-presenting cells. Thus T cells that responded to the same peptide-MHC competed with each other by lowering the amount of ligand with which the cells could react. As a result, the activation of high-affinity cells was favored. This provides a mechanism for the affinity maturation of a secondary T cell response.