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Title: Differential interleukin-10 expression in interferon regulatory factor-1 deficient mice during Plasmodium berghei blood-stage infection
Authors: Tan, R.S.-P.
Kara, A.U. 
Feng, C.
Asano, Y.
Sinniah, R.
Keywords: Interferon regulatory factor-1
Nitric oxide
Plasmodium berghei
Issue Date: 2000
Citation: Tan, R.S.-P., Kara, A.U., Feng, C., Asano, Y., Sinniah, R. (2000). Differential interleukin-10 expression in interferon regulatory factor-1 deficient mice during Plasmodium berghei blood-stage infection. Parasite Immunology 22 (9) : 425-435. ScholarBank@NUS Repository.
Abstract: Mice deficient of functional interferon regulatory factor-1 (IRF-1-/-) by targeted gene disruption infected with a lethal murine malaria strain, Plasmodium berghei ANKA survived longer than its wild-type littermates despite the inability to induce appreciable amounts of interferon-gamma (IFN-γ) and nitric oxide. In addition, infected IRF-1-/- mice displayed less organ injury with reduced necrosis and inflammation. Both wild-type and IRF-1-/- mice treated with exogenous interleukin-12 (IL-12) suffered extensive organ damage with corresponding up regulation of IFN-γ, suggesting the pathogenic potential of IL-12 and IFN-γ. IL-10 is a cytokine produced by CD4+ T lymphocytes belonging to the Th2 subset. Expression of IL-10 in the wild-type mice correlated with the severity of the infection, with higher mRNA expression towards the later stage of infection. In contrast to the wild-type mice, IL-10 levels in the IRF-1-/- mice were induced early in the infection and decreased gradually as the infection progressed. Both untreated and IL-12 treated wild-type mice appeared to follow a Th1-like immune response early in the infection and Th2-like immune response later in the infection. However, the IRF-1-/- mice were able to launch an altered immune response with a Th2-like immune response early in the infection. These findings suggest that IL-10 expression in the IRF-1-/- mice during the early stage of P. berghei ANKA infection could play an important role in suppressing pathogenic effects of a cell mediated immune response and promoting protective immunity against the parasite.
Source Title: Parasite Immunology
ISSN: 01419838
DOI: 10.1046/j.1365-3024.2000.00312.x
Appears in Collections:Staff Publications

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