In view of the clear documentation that T-cell function in the acquired immunodefiency syndrome (AIDS) is grossly impaired, the striking susceptibility of AIDS patients to infections caused by intracellular micro-organisms is not only not surprising but is predictable. Indeed, if one draws up a list of the pathogens against which successful host defense is thought to require an intact cell-mediated immune response (1) and compares this to a list of the pathogens which regularly infect patients with AIDS (2) (Table 1), the two lists are virtually superimposable. In addition, many of the AIDS pathogens are known to be intracellular organisms which, although capable of causing quite different clinical manifestations, share the common feature of being able to enter and replicate within unstimulated macrophages (1). In the presence of a normal, effective T cell-dependent immune response, however, presumed to be largely mediated by antigen-triggered lymphokine secretion with resultant macrophage activation, these same intracellular pathogens are killed or their growth is inhibited. Thus, the particular spectrum of opportunistic micro-organisms which consistently infect AIDS patients, the frequent failure of these patients to respond to appropriate antimicrobial therapy, their propensity for relapse despite adequate treatment, and the eventual uniformly fatal outcome of these infections all serve to graphically indicate that the process of macrophage activation in patients with AIDS is either profoundly disordered or more likely, has not taken place at all (3). Histopathologically, these clinical observations are expressed by the absence of granuloma formation, little or no inflammatory cell infiltrates, and overwhelming numbers of micro-organisms in wide-spread and numerous foci of tissue infection.