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Leukocyte accumulation at inflammatory sites probably involves chemotactic migration of the cells, and it is often presumed that abnormalities in cell accumulation derive from defective chemotaxis. The latter contention was examined by measuring the chemotactic response of leukocytes obtained from the circulation during conditions associated with depressed cellular inflammatory reactions. In two transplanted-tumor models induced by different chemical carcinogens in DA strain rats, monocyte chemotaxis was normal or enhanced while macrophage accumulation at inflammatory foci was severely curtailed. Late pregnancy in outbred Wistar rats depressed macrophage accumulation to peritoneal irritants while enhancing monocyte chemotaxis. Irritant-induced anti-inflammation (counterirritation) in Wistar rats decreased both polymorphonuclear leukocyte and macrophage accumulation during inflammation but enhanced the chemotactic activity of the corresponding cells obtained from the circulation. We concluded that in vitro chemotactic measurements were not predictive of cellular accumulation during inflammation in these conditions and that an intrinsic defect in chemotaxis was insufficient to explain anti-inflammation associated with cancer, pregnancy, or counterirritation.