The article of Kunisch et al discussing a cross reactivity of allegedly macrophage-specific anti-CD68 antibodies with fibroblasts and activated endothelial cells demonstrates amply that these antibodies should not be used for the identification of macrophages.¹ Yet they have been used for this purpose in nearly all medical disciplines, particularly in vascular diseases. In 1990 we observed that some neointimal cells in experimental transplantation atherosclerosis, human native atherosclerosis, and experimental native atherosclerosis had reacted with both presumptive macrophage-specific antibodies (RAM11, HAM56) and an antibody against muscle actin (HHF35).² In 1997, Andreeva et al demonstrated that the very same human intimal and neointimal cells were immunopositive, both with anti-macrophage (CD68, HAM56) and anti-muscle actin (asm-1, HHF35) antibodies.³ On the basis of these findings, these authors formed a hypothesis that the macrophage markers involved in these reactions were not indicative of cell histogenesis but of phagocytosis. Neither our observation² nor the demonstration of Andreeva et al³ had any influence on the practice of macrophage identification by the above mentioned antibodies.

Today, I share Kuhn’s opinion⁴ that the acceptance or rejection of new scientific ideas depends on their relationship to existing paradigms. If they are in agreement with them they are accepted, but if they contradict …