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Granulomatous Hypersensitivity to Schistosoma Mansoni Eggs in Thymectomized and Bursectomized Chickens¹

From the Division of Geographic Medicine, Department of Medicine, Case Western Reserve University and University Hospitals, Cleveland, Ohio

Abstract

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).

Footnotes

¹ This work was supported by the United States-Japan Cooperative Medical Science Program administered by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health Grant No. AI-08163.