Modulation of granulomatous hypersensitivity. II. Participation of Ly 1+ and Ly 2+ T lymphocytes in the suppression of granuloma formation and lymphokine production in <i>Schistosoma mansoni</i>-infected mice.

Abstract

The regulatory mechanism(s) active in the spontaneous suppression of parasite egg-induced granulomatous response was analyzed in Schistosoma mansoni-infected mice. A single injection of cyclophosphamide (CY) given to chronically infected mice with diminished granulomas and impaired ability to produce MIF restored the enhanced granulomatous response and lymphokine production by spleen cells. Drug-treated animals also showed a rise in the level of circulating anti-egg antigen antibody. After CY treatment, spleen cells were still capable of adoptively suppressing the vigorous granulomatous response and MIF production in acutely infected recipients. Adoptive suppression, however, was abrogated when spleen cells of chronically infected mice were pretreated with anti-Lyt 1.1 alloantiserum and C before transfer. Based on the present and previous observations, it is proposed that the modulated granulomatous inflammatory response in mice with chronic infection is maintained by a dynamic equilibrium between effector and regulator lymphocytes. Although the inflammation is maintained by Ly 1+ Ia- TDH cells, the intensity of the response is regulated by Ly 1+ Ia+ TH, Ly 2+ Ia+ Ts and possibly a putative precursor population of lymphocytes.