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IL-4 and IL-10 are essential for immunosuppression induced by high molecular weight proteins from Ascaris suum
The extract from Ascaris suum worms (Asc) impairs Th1 and Th2 responses to a non-related antigen, i.e. ovalbumin (OVA). Its suppressive capacity is due to high molecular weight components present in a gel filtration fraction (PI). This fraction is able to elicit IL-4 and IL-10 secretion. Interesting...
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Published in: | Cytokine (Philadelphia, Pa.) Pa.), 2004-10, Vol.28 (2), p.92-100 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The extract from
Ascaris suum worms (Asc) impairs Th1 and Th2 responses to a non-related antigen, i.e. ovalbumin (OVA). Its suppressive capacity is due to high molecular weight components present in a gel filtration fraction (PI). This fraction is able to elicit IL-4 and IL-10 secretion. Interestingly enough, it induces anti-PI non-anaphylactic IgG1 synthesis through the action of IL-12/IFN-γ. Here, we investigated the down-regulation of the immune response to OVA by PI in IL-12, IFN-γ, IL-4 or IL-10 C57BL/6 knockout mice immunized with OVA
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PI in adjuvant. OVA-induced delayed-type hypersensitivity (DTH) reactions, secretion of IL-2 and IFN-γ, and IgG1, IgG2c and IgE antibody production were suppressed by PI in wild-type mice, as well as in IL-12- or IFN-γ-deficient mice. In contrast, PI had no effect on anti-OVA IgE production and DTH, and induced only a partial suppression of IgG1 and IFN-γ in IL-10
−/− mice. The experiments also showed that IL-4 was involved in the PI-induced suppression of IgG2c antibodies and IL-2 secretion. Finally, down-regulation of IFN-γ was not seen in mice lacking both IL-4 and IL-10, i.e. IL-4
−/− mice treated with anti-IL-10 antibodies before immunization. These results exclude the participation of IL-12 and IFN-γ in PI-induced immunosuppression, and highlight the essential role of IL-10 in the suppression of OVA-specific Th2-related parameters, as well as the cooperation between IL-10 and IL-4 in the suppression of Th1-related parameters. |
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ISSN: | 1043-4666 1096-0023 |
DOI: | 10.1016/j.cyto.2004.07.004 |