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Immunology |
Johannes Gutenberg Universität, III. Medizinische Klinik, 55131 Mainz [B. S., U. W., C. H.]; Deutsches Krebsforschungsinstitut, 69720 Heidelberg [F. M.]; and Max Delbrück Centrum für Molekulare Medizin, 13122 Berlin, [T. B.] Germany
The murine B16 melanoma system represents an important in
vivo model for the evaluation of T cell-based immunization and
vaccination strategies, although deficient MHC class I surface
expression has been identified in these cells. We postulate here that
the MHC class I-deficient phenotype of B16 melanoma cells is
attributable to down-regulation or the loss of the expression and
function of multiple components of the MHC class I antigen-processing
pathway, including the peptide transporter associated with antigen
processing, the proteasome subunits LMP2, LMP7, and LMP10,
PA28
and -ß, and the chaperone tapasin. In contrast, calnexin,
calreticulin, ER60, and protein disulfide isomerase expression
are unaltered or only marginally suppressed in these cells. The level
of down-regulation of the components of the antigen-processing pathway
is either transcriptionally or posttranscriptionally controlled and
could be corrected in all cases by IFN-
treatment, which also
reconstituted MHC class I surface expression. Thus, B16 melanoma cells
can be used as a model for the characterization of the mechanisms
underlying the coordinated dysregulation of the antigen-processing
components, which should provide new insights into the development of
tumors and the factors controlling this process.
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