In addition to T and B cells, accessory cells such as macrophages are necessary for an immune response to occur. At present it is probably reasonable to regard collaborative immune response as a series of interrelated processes in which antigen-specific recognition is performed and in which various nonspecific mediators function as modifiers to regulate the intensity and quality of the response. According to this model, immunosuppressive drugs interfere at different stages and levels of the immune response. Glucocorticoids inhibit preferentially the activities of monocytes and T-helper cells as well as lymphokine production. Cyclosporin effectively inhibits the production of interleukin-2 and influences selectively the action of the T lymphocytes. Azathioprine, cyclophosphamide and methotrexate decrease the proliferative response of all the cells involved in the immune response. The immunosuppressive activity of chloroquine is still not well established, but the drug seems to have inhibitory effect on thromboxane and interleukin-2 production. Whole populations of lymphoid elements are destroyed by administering antibodies against surface determinants of these lymphoid elements. Antiidiotypic antibodies, present in intravenous immunoglobulin preparations from pools of donors, are capable of eliminating circulating (auto-)antibodies by binding to the idiotypic region of a specific disease-associated antibody.