Early studies in which immunoglobulin was found in the Schistosoma mansoni egg granuloma led to the assumption that antibody played a major etiologic role in the development of this lesion (1, 2). Subsequent investigations, however, revealed that granulomatous hypersensitivity to S. mansoni eggs could be passively transferred with cells and not with serum (3). Further studies confirmed the latter findings in that: 1) complete granulomas consisting largely of macrophages, eosinophils, and lymphocytes form in the absence of any detectable IgG1 or IgG2 antibodies (4, 5); 2) the onset of granuloma formation correlates with the development of delayed dermal reactivity and in vitro correlates of delayed hypersensitivity (4, 5); and 3) suppression of cell-mediated reactivity markedly diminishes granuloma formation (6–8) whereas suppression of antibody formation via x-irradiation (9) or Friend virus leukemia (8) has no effect. In spite of considerable evidence suggesting that the immunologic etiology of the S. mansoni granuloma is virtually wholly cell-mediated, claims for an important role for antibody have continued (10). Our previous demonstration that primary and secondary granuloma formation occurs around S. mansoni eggs injected into pigeons established the feasibility of studying granulomatous hypersensitivity in avian species (11). Thus we could turn, in the present investigation, to the classical means of separating cell-mediated and antibodymediated reactions, ablation respectively of the thymus and the bursa of Fabricius of chickens (12, 13).
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Davis et al. (1974) studied this question.