The term “activated macrophage” was introduced into the literature and employed extensively by Mackaness in the 1960s to describe the enhanced microbicidal activity of macrophages from animals with acquired immunity to infection with facultative, intracellular bacterial parasites. The notion that macrophages need to undergo functional modification in order to express resistance to infection with certain bacteria can be traced back to the writings of Metchnikoff at the turn of the century (1). It was subsequent studies of tuberculosis more than of any other infectious disease, however, that provided the evidence for the concept of a mechanism of cellular immunity based on the capacity of macrophages to acquire and to intrinsically express increased microbicidal mechanisms. The knowledge a) that a major visible aspect of the host response to tuberculosis consisted of the accumulation of macrophages at infective foci to form tubercles, b) that the tubercle bacillus is invariably engaged by and harbored inside macrophages, c) that secondary infection results in an accelerated rate of tubercle formation and in the destruction of the tubercle bacilli therein, and d) that all of these events proceed apparently without the participation of humoral antibody were sound reasons for postulating a mechanism of cellular immunity based on the intrinsic microbicidal powers of the macrophage.


This work was supported by Grant CA-16642 from the National Cancer Institute and AI-10351 from the National Institute of Allergy and Infectious Diseases.

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