title: Delayed hypersensitivity granuloma formation and modulation around Schistosoma mansoni eggs in vitro. II. Regulatory T cell subsets.
abstract: Schistosoma mansoni granuloma modulation was first described in an in vivo murine model of schistosomiasis and was characterized as a diminished cellular responsiveness to newly formed eggs in chronic infections. This phenomenon of modulation was studied using an in vitro model of granuloma formation. Negative selection procedures using anti-Lyt-1.2, 2.2, and Qa-1 sera and complement on spleen cell populations from normal or S. mansoni-infected C57BL/6 or (C57BL/6 X A/J)F1 mice were examined for their effect on in vitro granuloma formation or modulation. These data suggest that there is a Lyt-1+2-, Qa-1+ T cell present in chronically infected spleen cells that is capable of inducing feedback suppression. In addition, selective removal of a population of Lyt-1-2+ T cells from chronically infected spleen cells augmented the ability of that population to form granulomas in vitro. The selective removal of Lyt-1+2- cells ablated the ability of chronically infected spleen cells to form in vitro granulomas. Granuloma formation is primarily dependent on a population of Lyt-1+, Qa-1+ cells, and modulation is dependent on 2 populations, 1 acting directly (Lyt-1-2+) and the other through a (Lyt-1+2-, Qa-1+) feedback mechanism of suppression.
mesh_terms: D000208:Acute Disease; D000818:Animals; D000961:Antilymphocyte Serum / Q000494:pharmacology; D002469:Cell Separation; D002908:Chronic Disease; D003165:Complement System Proteins; D005260:Female; D006099:Granuloma / Q000276:immunology*; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D008297:Male; D051379:Mice; D008805:Mice, Inbred A; D008810:Mice, Inbred C57BL; D010063:Ovum / Q000276:immunology*; D012550:Schistosoma mansoni / Q000276:immunology; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology*
chemical_list: D000961:Antilymphocyte Serum; D003165:Complement System Proteins