Abstract
Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene‐induced fibrosarcoma (MC‐16) demonstrate suppressed responsiveness to phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non‐tumorous mice. A similar depression of PHA‐induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non‐competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 μg/mouse, IP) on an alternate day basis to groups of tumor‐bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 μg/ml) to cultures of spleen cells from these tumor‐bearing mice, as well as to DBA/1J mice bearing the Cloudman S‐91 melanoma, enhanced spleen‐cell responsiveness to mitogen‐induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen‐induced DNA synthesis of spleen cells from non‐tumor‐bearing animals. It is hypothesized that tumors, or tumor‐cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.