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,§
*
Institute of Immunology and Infectious Diseases, University of Verona, Verona, Italy;
Servizio/Cattedra di Immunologia, Ospedale S. Martino, Universitá di Genova, Genoa, Italy;
Unit of Cellular and Molecular Genetics, Advanced Biotechnology Center, Genoa, Italy; and
§
Department of Clinical and Biological Sciences, University of Pavia, Varese, Italy
The AIR-1-encoded CIITA transcriptional activator is
crucial for both constitutive and IFN-
-induced MHC class II gene
transcription. We show here that the MHC class II negative phenotype of
the human hepatocarcinoma cell lines Alexander and HepG2 remains
unmodified after treatment with IFN-, although MHC class I
expression is up-modulated. This correlates with absence of CIITA
mature transcripts. Transfection of an expressible CIITA cDNA in
Alexander cells resulted in a very high cell surface expression of all
three human class II subsets, HLA-DR, -DP and -DQ, indicating that
normally observed induction of CIITA expression by IFN- is probably
blocked, in the hepatocarcinoma cell lines, at the level of CIITA
transcription and not at the level of IFN- receptor binding and
signal transduction mechanisms. To assess whether MHC class II
expression on CIITA-transfected Alexander cells could have functional
relevance, we tested their capacity to present antigenic peptides to an
HLA-DR-restricted T cell line specific for a peptide of
Mycobacterium tuberculosis Ag85 protein. It was
found that the transfected cells could not only present the exogenously
supplemented peptide but also process Ag85 protein to generate the
specific epitope recognized by the HLA-DR-restricted T cell line.
Similar results were obtained with CIITA-transfected CFPAC-1 pancreatic
adenocarcinoma cells, which differed from Alexander cells in that they
were inducible by IFN-. These results suggest new strategies to act
on CIITA for increasing the potential of a tumor cell to present
putative tumor Ags to the immune system.
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