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Down‐Regulation of Macrophage I‐A Expression in Tumor‐Bearing Mice

During the subcutaneous growth of a highly metastatic mammary adenocarcinoma line, C3‐L4 in C3H/HeJ mice, there was a rapid decline in macrophage l‐A expression in vivo. The incidence of l‐A+ macrophage subset in the spleen declined from 90% to 10% or less within 5 days of tumor transplantation, with a parallel decline in their absolute number. l‐A expression in these cells remained suppressed for a long time until tumors became necrotic and ulcerated. In spite of a low incidence (15–20%) of l‐A+ macrophages in the normal peritoneal space, tumor transplantation caused a long‐lasting decline in their incidence to one‐fourth of the original level. Tumor‐associated macrophages were predominantly l‐A‐ throughout the tumor life span. Thus l‐A‐ macrophages dominated in all anatomical compartments in tumor‐bearing mice. Macrophage l‐A expression was substantially restored (spleen) or stimulated (peritoneal space and tumor) in tumor‐transplanted mice subjected to chronic indomethacin therapy in the drinking water, indicating a reversal of prostaglandin‐mediated down‐regulation of macrophage l‐A expression in situ. Concomitantly, this therapy caused regression of the primary tumors and prevented lung metastasis. These results are relevant to the understanding of tumor–host interactions and its exploitation for immunotherapy.