Subsets Invo lved in the P roduc t i on and Suppress ion of M i

In hepatosplenic schistosomiasis mansoni, the pathological effects can be largely attributed to the T lymphocyte-mediated granulomatous host response (1, 2). The chronic granulomatous inflammations terminate in reparative fibrosis, which can lead to portal hypertension, esophageal varices, bleeding, and death (3). Andrade and Warren (4, 5) first showed, that mice with chronic schistosomiasis at the late stage of the infection displayed a spontaneous diminution in granuloma size, with a corresponding improvement in the clinico-pathological parameters of the disease. Periodic injection of eggs has shown that whereas at 8 wk of the infection mice mounted large pulmonary granulomatous reactions, beyond 16 wk granuloma formation decreased significantly, thus indicating a desensitization process (6). Further analysis showed that this process entailed complex changes in the humoral and cell-mediated eggspecific immune responses as well as the lymphocyte dynamics of the infected mice. Thus, passive hemagglutination and passive cutaneous anaphylaxis tests showed an increase in the level of circulating anti-soluble egg antigen (SEA) 1 antibodies. In contrast, delayed footpad reaction of infected mice was abrogated, and no migration inhibition factor (MIF)or eosinophil stimulation promoter (ESP)-active lymphokines were produced by cultured lymphoid cells (7, 8). A change in the ratios of T:B lymphocytes was also demonstrable in the blood, lymphoid organs, and granulomas of the chronically infected mice (9). So far both humoraland cell-mediated regulatory mechanism have been considered to act in the modulation of the granulomatous response. Antibody-mediated afferent immunologic blockade ofgranuloma formation has been described by Pelley and Warren (10), and the presence and active synthesis of immunoglobulins and anti-SEA antibodies within liver granulomas has been reported (11, 12). On the cellular side, adoptive transfer of lymphoid cells from mice