Host defense mechanisms often appear to be inadequate following cryptococcal invasion (1-4). Significant antibody response has not been demonstrated with any regularity in man or experimental animals during torula infection. Furthermore, cellular response in cryptococcosis is frequently sparse. The apparent inadequacy of host antibody and cellular defenses during torula infection has been related to the presence of a large capsule, surrounding the cryptococcus cell, which consists primarily of several polysaccharides (5).Benham (6) was able to produce antibodies to cryptococci in rabbits only after the capsule had been removed with hydrochloric acid. Evans and Kessel (7,8) and Neill, CastiUo, Smith, and Kapros (9), however, demonstrated precipitating and agglutinating antibodies in the rabbit following immunization with large numbers of heat-or formalin-killed cryptococci. These antibodies were dearly shown to be directed against the capsular material. The rabbit does not ordinarily develop progressive cryptococcosis so that no inference could be drawn as to the protective effect of such immunization in this animal.In recent studies, Gadebusch (10) reported that he could delay death in mice following cryptococcal challenge by the administration of immune rabbit serum. These as yet unconfirmed studies suggested that immune rabbit serum not only contained antibody directed against the cryptococcal capsule, but also was able to modify the course of a lethal cryptococeal infection. However, the challenge organisms were suspended in mucin, and the antisera and challenge were both given intraperitoneaUy within 2 hours of each other. It is quite possible that the apparent protection was related to dumping of fungi by the agglutinating antisera, thus in actuality reducing the size of the inoculum. Furthermore, mucin itself can at first reduce and later increase resistance non-specifically to many infections (11). Thus temporary dumping of fungus cells by antisera might retard the acute infection long enough to allow nonspecific resistance to develop.Gadebusch (12) also reported that death was delayed in mice infected with a lethal