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The Journal of Immunology, 1979, 123: 507-514.
Copyright © 1979 by The American Association of Immunologists, Inc.
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Carrier Effect During the Course of Experimental Schistosomiasis: Suppression of the Response to TNP-Schistosomula in Rats and Inbred Mice

F. Juarez Ramalho-Pinto1, S. Ronald Smithers2 and John H. L. Playfair

From the Division of Parasitology, National Institute for Medical Research, Mill Hill, London NW7 1AA, and Middlesex Hospital Medical School, London W1

Abstract

The helper T cell response of the mouse and rat to infection with Schistosoma mansoni was measured by using schistosomula as a carrier for the hapten TNP. After infection, both hosts showed a high level of helper T cell activity with a peak response between 8 to 10 days after exposure to cercariae. As infection progressed and protective immunity developed, there was a steady decline in the level of helper T cell activity as detected by the anti-TNP assay, and the response could not be restimulated by a second infection. Mice vaccinated with 30 formalin-fixed schistosomula gave a helper T cell response equivalent to that of infected mice, but their response remained at a high level for at least 24 weeks. Antibody to schistosomula was detected in the serum of mice 5 weeks after infection and reached high titers by week 11; no antibody was detected in vaccinated mice. The passive transfer of serum from 8- to 13-week infected mice reduced the PFC response after injection of TNP-schistosomula in 8- to 10-day infected mice and in vaccinated animals, suggesting that anti-carrier antibody was responsible for the depression of helper T cell activity. IgG purified from the serum of 16- to 17-week infected mice by affinity chromatography with a Sepharose-protein A gel specifically suppressed T cell cooperation to the schistosomular surface. The decline in helper T cell activity in schistosome-infected mice may not indicate a decrease in the number of helper T cells to schistosomula in chronically infected animals, but could reflect the blocking by anti-carrier antibody of the cooperation between T cells and the hapten-committed B cells.

Footnotes

1 F. J. R-P was supported by Conselho Nacional de Desenvolvimento Cientifico e Tecnológico (Brasil). Present address: Department of Biochemistry-Immunology, ICB, U.F.M.G., 30000 Belo Horizonte, MG Brazil.

2 Reprint requests: Dr. S. R. Smithers, National Institute for Medical Research, Mill Hill, London NW7 1AA.






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