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Relationship between the production of interferon-α/β and interferon-γ during acute toxoplasmosis

Published online by Cambridge University Press:  06 April 2009

B. Diez ,
A. Galdeano ,
R. Nicolas  and
R. Cisterna
B. Diez
Affiliation:
Department of Microbiology and Immunology, Basque Country University, Apartado 699, Bilbao, Spain
A. Galdeano
Affiliation:
Department of Microbiology and Immunology, Basque Country University, Apartado 699, Bilbao, Spain
R. Nicolas
Affiliation:
Department of Microbiology and Immunology, Basque Country University, Apartado 699, Bilbao, Spain
R. Cisterna
Affiliation:
Department of Microbiology and Immunology, Basque Country University, Apartado 699, Bilbao, Spain
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Summary

Acute toxoplasmosis was induced in mice, and interferon (IFN) production in serum and by spleen cells was evaluated during the infection period. Interferon was characterized by acid-treatment and anti-IFN-α/β neutralization. In order to verify the correlation between the unusual aspects of the IFN production and the induction of immunosuppression, splenocyte mitogen responsiveness was investigated concomitantly to IFN synthesis. The activity of Toxoplasma-induced serum IFN-α/β increased gradually throughout all post-infection days, but IFN-γ was not detected in the systemic circulation at any time during the infection. It was also observed that IFN-α/β production and the capacity to produce IFN-γ by spleen cells were closely and inversely correlated. As the infection progressed, more IFN-α/β was produced, and the ability of spleen cells to produce IFN-γ decreased. The observation that Toxoplasma-infected mice were concomitantly immunosuppressed (as documented by mitogen unresponsiveness and defective IFN-γ production) in direct correlation to IFN-α/β production, suggests that such IFN-α/β production is an important factor associated with acute toxoplasmosis-induced immunosuppression.

Keywords

toxoplasmosisinterferonsimmunosuppressionToxoplasma gondii.
Type
Research Article
Information
Parasitology , Volume 99 , Issue 1 , August 1989 , pp. 11 - 15
Copyright
Copyright © Cambridge University Press 1989

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