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- W1674162913 endingPage "3762" @default.
- W1674162913 startingPage "3757" @default.
- W1674162913 abstract "MRL lpr/lpr mice spontaneously develop a severe autoimmune lupus syndrome characterized by strong autoantibody production and massive lymphoproliferation, in which IFN-gamma plays a major pathogenic effect. The role of the IFN-gamma-inducing cytokine IL-18 in the autoimmune syndrome of lpr/lpr mice has been investigated. In response to IL-18, lymph node cells of lpr/lpr mice produce significant amounts of IFN-gamma and proliferate more potently as compared with cells from +/+ mice. Cells likely responsible for such hyperresponsiveness to IL-18 include NK cells and the CD4(+)/CD8(+) self-reactive T lymphocytes characteristically present in lymph nodes of lpr/lpr mice. Analysis of the expression of IL-18R complex revealed that mRNA for the IL-18R alpha-chain is constitutively expressed at similar level both in +/+ and lpr/lpr lymphocytes. In contrast, the expression of the accessory receptor chain IL-18R beta is low in unstimulated +/+ cells but significantly high in lpr/lpr cells. Thus, the abnormally high expression of the IL-18R chain IL-18R beta could be one of the causes of the hyperresponsiveness of lpr/lpr cells to IL-18 at the basis of consequent enhancement of IFN-gamma production and development of IFN-gamma-dependent autoimmune pathology." @default.
- W1674162913 created "2016-06-24" @default.
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- W1674162913 date "2001-03-15" @default.
- W1674162913 modified "2023-09-27" @default.
- W1674162913 title "Lymphocytes from Autoimmune MRL<i>lpr/lpr</i>Mice Are Hyperresponsive to IL-18 and Overexpress the IL-18 Receptor Accessory Chain" @default.
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- W1674162913 doi "https://doi.org/10.4049/jimmunol.166.6.3757" @default.
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