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Proinflammatory responses induced by Plasmodium falciparum glycosylphosphatidylinositols (GPIs) are thought to be involved in malaria pathogenesis. In this study, we investigated the role of MAPK-activated protein kinase 2 (MK2) in the regulation of tumor necrosis factor-α (TNF-α) and interleukin (IL)-12, two of the major inflammatory cytokines produced by macrophages stimulated with GPIs. We show that MK2 differentially regulates the GPI-induced production of TNF-α and IL-12. Although TNF-α production was markedly decreased, IL-12 expression was increased by 2–3-fold in GPI-stimulated MK2^−/− macrophages compared with wild type (WT) cells. MK2^−/− macrophages produced markedly decreased levels of TNF-α than WT macrophages mainly because of lower mRNA stability and translation. In the case of IL-12, mRNA was substantially higher in MK2^−/− macrophages than WT. This enhanced …