I N M I C E *

Resistance to infection with intracellular bacteria such as Listeria monocytogenes is cell-mediated and requires the participation of both lymphoid cells and mononuclear phagocytes (1). During the course of a nonlethal infection there arises a population of specifically sensitized lymphocytes that are capable of passively transferring immunity to normal mice (2). This passive transfer requires the accumulation of recipient macrophages at the sites of Listeria infection, for it is the macrophage which is the ultimate effector cell that rids the host of the bacteria (3). Once activated by the specifically sensitized lymphocytes in the presence of Listeria antigen, the macrophages act nonspecifically, i.e., they will protect against infection with an unrelated bacterial pathogen (3, 4). The mechanism of activation of macrophages by lymphocytes is not known, but may be through the release of one or more of the lymphokines, as described for in vitro correlates of delayed hypersensitivity (5, 6). Prendergast and Suzuki (7) have described a protein having a tool wt of 32,000, isolated from the coelomocytes of the sea star (Asteriasforbesi), that acts in a manner analogous to the mediators of delayed hypersensitivity. This sea star factor (SSF) 1 has the following characteristics: (a) it causes a skin reaction in nonsensitized guinea pigs which is identical both temporally and cytologically to a delayed hypersensitivity-type skin reaction; (b) it inhibits the migration of normal guinea pig macrophages from capillary tubes; (c) it is chemotactic for macrophages; and (d) macrophages treated either in vivo or in vitro with SSF are morphologically altered to an "activated" form (8, 9).