Carrier-dependent suppression of the anti-phosphorylcholine plaque-forming cell response in Trichinella-infected mice is mediated by anti-hapten IgG1 antibodies.

In normal mice, the phosphorylcholine(PC)-bearing Trichinella spiralis antigen FCp induces PC-specific IgM antibodies. Infection with T. spiralis appears to suppress this response, without affecting the production of anti-PC antibodies in response to other PC-bearing antigens; the suppression can thus be considered carrier-dependent. Previous work in our laboratory has indicated that the observed suppression is due to a soluble factor present in the serum of infected mice. In the work reported here, we investigated the identity of this factor. After in vitro stimulation with FCp, spleen cells from FCp-primed infected mice showed a stronger anti-PC IgM response than spleen cells from FCp-primed uninfected mice, confirming that cell memory for FCp is unimpaired by infection. Passive transfer of serum from infected mice to normal recipients, followed by immunization of recipients with FCp or another thymus-dependent or thymus-independent PC-bearing antigen, confirmed that the suppressive agent is soluble and that its activity is carrier-dependent. The suppressive agent was retained by immunoaffinity chromatography with PC or rabbit anti-mouse Ig as ligand, showing that it is a PC-specific Ig. Gel filtration of the fractions retained by PC-immunoaffinity, and subsequent identification of Ig isotypes by an ELISA-based procedure, indicated that the suppressive Igs are of the IgG1 isotype. These findings may be relevant for understanding antibody-mediated down-regulation of the immune response.