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Evaluation of the Potential Role of Class II Histocompatibility Antigen HLA-DR in Platelet/Tumor Cell Interaction

Department of Experimental Medicine, University of Rome La Sapienza [P. F., F. M., P. P. G.], Viale Regina Elena 324, and Regina Elena Cancer Institute [F. G., A. S.], Viale Regina Elena 291, 00161 Rome, Italy

It has been reported that HLA-DR is a potent inducer of thrombin generation. Human colorectal cells (GEO, WiDr, DLD-1, and MIP) that lack the constitutive expression of HLA-DR cause platelet aggregation through a thrombin-dependent mechanism. Treatment with recombinant human -interferon induced the expression of HLA-DR in the GEO, WiDr, and DLD-1 cells, whereas the MIP cell line remained HLA-DR negative. The concurrent analysis of tumor cell/platelet interaction after -interferon treatment showed a decrease in platelet proaggregating activity of either the responsive GEO (highly expressing HLA-DR) or the unresponsive MIP (HLA-DR negative) cells. Furthermore, the DLD-1 (moderately expressing HLA-DR) cells showed an increase of proaggregating activity after -interferon treatment, whereas WiDr (highly expressing HLA-DR) cells did not modify their activity. These results suggest a lack of a role of HLA-DR in the in vitro platelet proaggregating activity of human colorectal tumor cells.

¹ To whom requests for reprints should be addressed.

Received 10/ 1/93. Accepted 12/15/93.