Atrophy of the thymic cortex in mice with granulomatous schistosomiasis mansoni.

Thymic histopathology and granulomatous hypersensitivity were examined in CBA/J mice infected with varying numbers of Schistosoma mansoni worms. At the acute phase (8 weeks) of infection, the thymi of infected mice showed depletion of cortical lymphocytes that resulted in loss of distinction in the corticomedullary region. The degree of cortical depletion correlated directly with the intensity of infection, as assessed by total egg burden of the liver. Adrenalectomy of heavily infected mice 5 to 6 weeks after infection did not alter the course of cortical lymphocyte depletion. Thymus mass was diminished by as much as 80% in heavily infected mice. However, the thymi of lightly infected mice which survived 20 weeks of infection did not differ in histology or total tissue mass from age-matched uninfected controls. Adult thymectomy at 3 weeks of infection did not abrogate the spontaneous modulation (diminution) of granuloma formation in 20-week infected mice, although spleen cells from these mice failed to adoptively transfer suppression. Heavily infected mice which did not survive beyond the acute phase (8 to 9 weeks) of infection displayed a diminished granulomatous response that was partially restored by thymectomy carried out at 5 to 6 weeks of infection. Spleen cells from heavily infected mice (8 weeks) adoptively suppressed the granulomatous response in lightly infected recipients. It is concluded that histological changes observed in the thymus concurrent with egg dissemination and granulomatous hypersensitivity correlated with T cell-mediated regulatory events.