Modulation of Schistosoma mansoni egg-induced granuloma formation: I-J restriction of T cell-mediated suppression in a chronic parasitic infection.

Abstract

Newly formed hepatic granulomas around S. mansoni eggs become progressively smaller during the chronic (.gtoreq. 15 wk after infection) phase of the disease. This reduction in granuloma size, termed modulation, is caused in part by a T lymphocyte that can adoptively transfer modulation to 6 wk infected mice. A possible role for the I-J locus in regulating the suppressor T lymphocyte aspects of modulation was investigated. Adoptive transfer between congeneic B10.A(3R) and B10.A(5R) mice (differing at the I-J locus) indicated that optimal suppression is dependent upon homology at the I-J locus. In vivo treatment of chronically infected mice with microliter amounts of antiserum specific for the recipient''s I-J determinant blocked modulation during chronic infection and prevented adoptive transfer of suppression to 6 wk infected mice. The in vivo regimen of anti-I-J had no effect on anti-schistosomal egg antigen titers during chronic infection. These results demonstrate an I-J restriction for suppression. Probably, the suppressor T lymphocyte circuit responsible for this aspect of modulation requires an I-J-positive lymphocyte.