| Research Abstract |
IL-18 plays important roles throughout immune reactions. We had revealed that, IL-18 deficient mice deteriorated pathogenesis of Plasmodium infection and exogenious IL-18 improved the disease (Shin R.P., Kashiwamura S. et al., J.Immunol.,2002). Further we had reported IL-18 could induced IL-4, IL-10 and IL-13 productions from T cells, NK cells and Mast cells (Kashiwamura S. et al., J.Immunothera.,2002). Moreover, we had reported IL-18 production in patients of endometoriosis and non-immune parenchymal cells produced PGE2 in response to IL-18 stimulation (Oku H., Tsuji Y., Kashiwamura S. et al., Hum Reprod., 2004).
In current study, we had revealed that IL-18 could prevent pathological changes in bleomycine-induced lung injury and caerulein-induced acute pancreatitis (Nakatani-Okuda A., Ueda H., Kashiwamura S. et al., Am.J. Physiol.Lung.Cell Mol. Physiol., 2005) (Ueno N., Kashiwamura S. et al., Shock, 2005). Our data strongly suggested the possibility that, NO or PGE2 induced by IL-18 suppress TNF-α production both in infectious disease and autoimmune diseases (Okamura H., Kashiwamura S., Ueda H., Nippon Rinsho, 2005).Further, we had revealed stress induced super-oxide induced IL-18 production through activation of Caspase-1 (Sekiyama A., Ueda H., Kashiwamura S. et al., Immunity, 2005)
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