Abstract
For many years it has been known that serum from immune animals would passively transfer anaphylactic sensitivity and resistance to the lethal effects of certain toxins to nonimmune recipients. However, attempts to transfer other responses such as delayed cutaneous hypersensitivity or contact allergy to nonimmune recipients with immune sera were unsuccessful. It was not until 1942 that Landsteiner and Chase1 discovered that it was possible to transfer reactivity to simple chemicals by injecting lymphoid cells from immune donors into nonimmune recipients. These experiments laid the foundation for cellular immunology. Subsequent experiments2,3 defined two important properties of this phenomenon in laboratory animals. First, it was essential to use intact, living cells from immune donors. Dead or disrupted cells or living cells from nonimmune recipients were not effective. Second, a persisting state of sensitivity in the recipient was obtained only when a syngeneic relationship existed between the donors and recipients. Although transfers between allogeneic donor-recipient pairs were successful, the duration of the sensitive state was brief, presumably because the recipients rejected the donor's cells.