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Interleukin‐10 modulates susceptibility in experimental cerebral malaria
Author(s) -
KOSSODO S.,
MONSO C.,
JUILLARD P.,
VELU T.,
GOLDMAN M.,
GRAU G. E.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00290.x
Subject(s) - plasmodium berghei , cerebral malaria , in vivo , tumor necrosis factor alpha , malaria , spleen , biology , endogeny , immunology , interferon gamma , in vitro , recombinant dna , interleukin , cytokine , plasmodium falciparum , endocrinology , biochemistry , microbiology and biotechnology , gene
In this study, we examined the effects of interleukin‐10 (IL‐10) on the outcome of experimental cerebral malaria (CM), a lethal neurological syndrome that occurs in susceptible strains of mice after infection with Plasmodium berghei ANKA (PbA). Constitutive IL‐10 mRNA levels were significantly higher in the spleen and brain of resistant animals. In vivo neutralization of endogenous IL‐10 in CM‐resistant mice induced the neurological syndrome in 35·7% of these mice, as opposed to 7·7% in controls. IL‐10 inhibited PbA antigen‐specific interferon‐ & gamma; (IFN‐ & gamma;) production in vitro but not tumour necrosis factor (TNF) serum levels in vivo . Susceptible mice, on the other hand, were significantly protected against CM when injected with recombinant IL‐10. Overall, our findings suggest that IL‐10 plays a protective role against experimental cerebral malaria.