Central nervous system (CNS) tumours possess special immunological features resulting from their development in an organ having a privileged immunological status. The following review gives a summary of actual data concerning their tumour-associated antigens, the immunological responses of their hosts and the mechanisms permitting them to escape from these responses. There is presently no proof of the existence of tumour-specific antigens on spontaneous glial tumours. Much progress has been made in this area with the development of monoclonal antibodies technology which mainly disclosed the profound antigenic heterogeneity of brain tumours. This heterogeneity could favour the escape of brain tumours from immunosurveillance; furthermore, it represents a major limitation to the use of monoclonal antibodies for diagnosis or therapy. Regarding the immunological responses of brain tumour patients, the main feature is a profound depression of cellular immunity creating an anergic state toward a large number of antigens. In vitro, it concerns specifically T4 helper lymphocytes: their mitogenic responses and secretion of interleukin-2 after antigenic stimuli are drastically reduced. Three phenomena have also been incriminated to explain the defect of immunosurveillance in brain tumour patients: 1) the synthesis by tumour cells of a protective mucopolysaccharidic coat, 2) the secretion by these cells of specific immunosuppressive factors related to cytokines, 3) the isolation of CNS maintained by the blood-brain barrier which regulates the circulation of immunocompetent cells between the intra- and extracerebral compartments. Currents efforts are focused on the individualization of therapy based on these biologic principles.