The immune response is characterized by its high degree of specificity. B lymphocytes capable of producing antibodies that react with an antigen are selected to proliferate and to difierentiate as a result of their binding antigens that are directly stimulatory (Moller 1975) and as a result of their presentation of antigens to antigen-specific helper T lymphocytes (Noelle & Snow 1991). T lymphocytes similarly are selected to proliferate and to differentiate as a result of signals received when they are presented with an antigen-derived peptide/self MHC complex by antigen-presenting cells, such as B lymphocytes, dendritic cells or macrophages (Lanzavecchia 1990). Specificity of the immune response is maintained because only those lymphocytes that are capable of reacting with a determinant on the immunogen are induced to clonally expand and differentiate into mature effector cells.

There is, however, a second, less completely understood aspect to immune specificity. Different effector mechanisms are recruited in response to different antigens or pathogens. In the mouse, for example, viral infections typically induce antibody responses of the IgG2a isotype (Coutelier et al. 1987), and are accompanied by activation of macrophages and the generation of cytotoxic T lymphocytes (Leist et al. 1989). In contrast, helminth parasites typically