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Article: Levamisole induces interleukin-18 and shifts type 1/type 2 cytokine balance

TitleLevamisole induces interleukin-18 and shifts type 1/type 2 cytokine balance
Authors
Issue Date2000
Citation
Immunology, 2000, v. 100 n. 2, p. 217-224 How to Cite?
AbstractImmune responses can be classified, according to the predominant cytokines involved, into type 1 (featuring interferon-γ, IFN-γ) and type 2 (featuring interleukin-4, IL-4); imbalance between type 1 and type 2 cytokine compartments has been implicated in many human diseases. Levamisole is a drug with an unknown mode of action that has been used to boost immunity in infectious diseases including leprosy, and in some cancers. To test the hypothesis that levamisole acts by inducing a shift to a type 1 immune response, we used Brown Norway (BN) rats, which are markedly biased to type 2 responses. BN rats treated with levamisole showed a dose-dependent rise in serum IFN-γ and fall in serum immunoglobulin E (IgE) level. Detailed analysis of cytokine gene expression showed upregulation of IFN-γ and downregulation of IL-4 messenger RNA. This coincided with marked upregulation of IL-18, a recently characterized cytokine with potent activity in stimulating IFN-γ production. IL-12 was not induced. Further, the type 2 response induced in BN rats by mercuric chloride was markedly attenuated when rats were pretreated with levamisole: there was a 2-log reduction in maximum serum IgE level and marked attenuation of IL-4 gene upregulation. These data indicate that levamisole acts by resetting the immune balance towards a type 1 response via induction of IL-18. Our findings provide a direction for development of more specific immunomodulating therapy.
Persistent Identifierhttp://hdl.handle.net/10722/195361
ISSN
2015 Impact Factor: 4.078
2015 SCImago Journal Rankings: 2.038
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSzeto, C-C-
dc.contributor.authorGillespie, KM-
dc.contributor.authorMathieson, PW-
dc.date.accessioned2014-02-28T06:12:02Z-
dc.date.available2014-02-28T06:12:02Z-
dc.date.issued2000-
dc.identifier.citationImmunology, 2000, v. 100 n. 2, p. 217-224-
dc.identifier.issn0019-2805-
dc.identifier.urihttp://hdl.handle.net/10722/195361-
dc.description.abstractImmune responses can be classified, according to the predominant cytokines involved, into type 1 (featuring interferon-γ, IFN-γ) and type 2 (featuring interleukin-4, IL-4); imbalance between type 1 and type 2 cytokine compartments has been implicated in many human diseases. Levamisole is a drug with an unknown mode of action that has been used to boost immunity in infectious diseases including leprosy, and in some cancers. To test the hypothesis that levamisole acts by inducing a shift to a type 1 immune response, we used Brown Norway (BN) rats, which are markedly biased to type 2 responses. BN rats treated with levamisole showed a dose-dependent rise in serum IFN-γ and fall in serum immunoglobulin E (IgE) level. Detailed analysis of cytokine gene expression showed upregulation of IFN-γ and downregulation of IL-4 messenger RNA. This coincided with marked upregulation of IL-18, a recently characterized cytokine with potent activity in stimulating IFN-γ production. IL-12 was not induced. Further, the type 2 response induced in BN rats by mercuric chloride was markedly attenuated when rats were pretreated with levamisole: there was a 2-log reduction in maximum serum IgE level and marked attenuation of IL-4 gene upregulation. These data indicate that levamisole acts by resetting the immune balance towards a type 1 response via induction of IL-18. Our findings provide a direction for development of more specific immunomodulating therapy.-
dc.languageeng-
dc.relation.ispartofImmunology-
dc.titleLevamisole induces interleukin-18 and shifts type 1/type 2 cytokine balance-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2567.2000.00042.x-
dc.identifier.pmid10886398-
dc.identifier.scopuseid_2-s2.0-0034120590-
dc.identifier.volume100-
dc.identifier.issue2-
dc.identifier.spage217-
dc.identifier.epage224-
dc.identifier.isiWOS:000087487500010-

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