Inhibition of lung colonization of mouse colon 26 adenocarcinoma by recombinant mouse interferon ? through a modification of platelet function

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Abstract
Recombinant murine interferon β (MuIFN-β) given i.v. efficiently inhibited both pulmonary arrest and formation of lung colonies of NL-17, a highly metastatic variant of mouse colon adenocarcinoma 26. NL-17 was rather resistant to MuIFN-β in vitro and was highly resistant to natural killer cells of mice even though they were treated in vivo with MuIFN-β. Platelets isolated from MuIFN-β-treated mice showed reduced aggregating activity induced by NL-17. Since lung colonization by NL-17 is influenced by platelet aggregation, the inhibition of colonization by MuIFN-β could be partly mediated through modification of platelet function in vivo. The effect of MuIFN-β on platelet function and its subsequent inhibition of lung colony formation give new insights into the action of recombinant MuIFN-β.