Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

Turnover of Ia-Peptide Complexes is Facilitated in Viable Antigen-Presenting Cells: Biosynthetic Turnover of Ia vs. Peptide Exchange

Clifford V. Harding, Richard W. Roof and Emil R. Unanue
Proceedings of the National Academy of Sciences of the United States of America
Vol. 86, No. 11 (Jun. 1, 1989), pp. 4230-4234
Stable URL: http://www.jstor.org/stable/33659
Page Count: 5
  • Read Online (Free)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Turnover of Ia-Peptide Complexes is Facilitated in Viable Antigen-Presenting Cells: Biosynthetic Turnover of Ia vs. Peptide Exchange
Preview not available

Abstract

Macrophages and B cells process antigens to produce antigenic peptides that associate with class II major histocompatibility complex molecules (e.g., Ia molecules); these Ia-peptide complexes are recognized by CD4+ T lymphocytes. Processing of the antigen hen egg white lysozyme was inhibited by cycloheximide in peritoneal exudate cells (PECs, largely macrophages), but not in TA3 B-lymphoma cells. The uptake and metabolism of hen egg white lysozyme was largely intact in cycloheximide-treated PECs, implicating a blockade in other steps in the formation of Ia-peptide complexes. Turnover of Ia-peptide complexes was markedly enhanced in viable antigen-presenting cells (TA3 and PEC) as compared to such complexes studied on fixed cells or in isolated preparations of Ia and peptide. In B cells the half-life of Ia-peptide complexes was much shorter than the half-life of the Ia molecules, implying turnover of Ia-peptide complexes by dissociation and peptide exchange. In PECs, the dissociation of Ia-peptide complexes was more limited; the enhanced Ia-peptide turnover in viable PECs reflected in part biosynthetic turnover of Ia molecules. Specific mechanisms may exist in TA3 cells to facilitate exchange of peptides bound to Ia, allowing recycling of Ia to present another antigenic peptide; such Ia recycling would explain the ability of these cells to process and present antigen in the absence of Ia synthesis.

Page Thumbnails

  • Thumbnail: Page 
4230
    4230
  • Thumbnail: Page 
4231
    4231
  • Thumbnail: Page 
4232
    4232
  • Thumbnail: Page 
4233
    4233
  • Thumbnail: Page 
4234
    4234