Participation of Basophilic Leukocytes and Macrophage Aggregates* by Harold F. Dvorak,$ Ann M. Dvorak, and Winthrop

An association has been established between cell-mediated hypersensitivity and specific resistance to tumors in many species including man (1-10). Humoral immunity is apparently less important in the rejection of solid neoplasms and may actually enhance tumor growth (3, 8, 9). Tumor resistance requires lymphocytes sensitized against tumor-specific transplantation antigens, but the means by which these cells effect tumor cell destruction in vitro or in vivo is not yet established. The mechanisms that have been proposed for immunologic tumor rejection are largely based on model systems in which defined cell populations or their products are incubated with tumor cells in vitro. Evidence has been presented that "killer" lymphocytes exert a direct cytopathic effect requiring contact with tumor target cells (11-13) and alternatively that lymphocytes act less directly, either by secreting cytotoxic mediators such as lymphotoxin (13-15) or by attracting and stimulating the function of other immunologically nonspecific cells, particularly macrophages (16). As useful as these models have been in elucidating the potential capabilities of lymphocytes and macrophages, they may not reflect the actual mechanism(s) by which the sensitized host rejects tumors in vivo. A further complication to an understanding of immunologic mechanisms of tumor destruction has been the discovery in recent years that cellular hypersensitivity itself is not a homogeneous entity. We have shown that several forms of delayed-onset, lymphocyte-mediated hypersensitivity in animals and man are characterized by substantial infiltrations of basophilic leukocytes; these have been designated "cutaneous basophil hypersensitivity" (CBH) 1 to distinguish them from classic tuberculin hypersensitivity in which basophils are rare (17-23). At present, CBH-type reactions