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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 1981 Feb;78(2):1152–1156. doi: 10.1073/pnas.78.2.1152

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

W F Green, D G Colley
PMCID: PMC319965  PMID: 6972040

Abstract

Newly formed hepatic granulomas around Schistosoma mansoni eggs become progressively smaller during the chronic (greater than or equal to 15 weeks after infection) phase of the disease. This reduction in granuloma size, termed "modulation," is known to be caused in part by a T lymphocyte that can adoptively transfer modulation to 6-week-infected mice. The present study examines a possible role for the I-J locus in regulating the suppressor T lymphocyte aspects of modulation. 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-week-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. It appears that the suppressor T lymphocyte circuit responsible for this aspect of modulation requires an I-J positive lymphocyte.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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