Linked Life Data

12594855

Source:http://linkedlifedata.com/resource/pubmed/id/12594855

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pubmed-article:12594855pubmed:abstractTextTapasin is a member of the MHC class I loading complex where it bridges the TAP peptide transporter to class I molecules. The main role of tapasin is assumed to be the facilitation of peptide loading and optimization of the peptide cargo. Here, we describe another important function for tapasin. In tapasin-deficient (Tpn(-/-)) mice the absence of tapasin was found to have a dramatic effect on the stability of the TAP1/TAP2 heterodimeric peptide transporter. Steady-state expression of TAP protein was reduced more than 100-fold from about 3 x 10(4) TAP molecules per wild-type splenocyte to about 1 x 10(2) TAP per Tpn(-/-) splenocyte. Thus, a major function of murine tapasin appears to be the stabilization of TAP. The low amount of TAP moleculesin Tpn(-/-) lymphocytes is likely to contribute to the severe impairment of MHC class I expression. Surprisingly, activation of Tpn(-/-) lymphocytes yielded strongly enhanced class I expression comparable to wild-type levels, although TAP expression remained low and in the magnitude of several hundred molecules per cell. The high level of class I on activated Tpn(-/-) cells depended on peptides generated by the proteasome as indicated by blockade with the proteasome-specific inhibitor lactacystin. Lymphocyte activation induced an increase in ubiquitinated proteins that are cleaved into peptides by the proteasome. These findings suggest that in the presence of a large peptide pool in the cytosol, a small number of TAP transporters is sufficient to translocate enough peptides for high class I expression. However, these class I molecules were less stable than those of wild-type cells, indicating that tapasin is not only required for stabilization of TAP but also for optimization of the spectrum of bound peptides.lld:pubmed
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pubmed-article:12594855pubmed:articleTitleA major role for tapasin as a stabilizer of the TAP peptide transporter and consequences for MHC class I expression.lld:pubmed
pubmed-article:12594855pubmed:affiliationDeutsches Krebsforschungszentrum Heidelberg, Abteilung Molekulare Immunologie, Heidelberg, Germany.lld:pubmed
pubmed-article:12594855pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12594855pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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