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Haruki Okamura

Researcher at Hyogo College of Medicine

Publications -  235
Citations -  20818

Haruki Okamura is an academic researcher from Hyogo College of Medicine. The author has contributed to research in topics: Interleukin 12 & Cytokine. The author has an hindex of 63, co-authored 231 publications receiving 19774 citations.

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Cloning of a new cytokine that induces IFN-gamma production by T cells.

TL;DR: The cloning of a recently identified IFN-γ-inducing factor (IGIF) that augments natural killer activity in spleen cells and may be involved in the development of Thl cells and also in mechanisms of tissue injury in inflammatory reactions is reported.
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Interleukin-18 regulates both Th1 and Th2 responses.

TL;DR: IL-18 is a potent proinflammatory cytokine that has pathophysiological roles in several inflammatory conditions, and in principle, IL-18 enhances the IL-12-driven Th1 immune responses, but it can also stimulate Th2 immune responses in the absence of IL- 12.
Journal Article

IL-12 up-regulates IL-18 receptor expression on T cells, Th1 cells, and B cells: synergism with IL-18 for IFN-gamma production.

TL;DR: It is shown that IL-12 and IL-18 promptly and synergistically induce T and B cells to develop into IFN-gamma-producing cells without engaging their Ag receptors and the mechanism underlying differences inIL-18 responsiveness between Th1 and Th2 cells is studied.
Journal Article

Cloning of the cDNA for human IFN-gamma-inducing factor, expression in Escherichia coli, and studies on the biologic activities of the protein.

TL;DR: It is proposed that this novel cytokine be designated as IL-18 based on the pleiotropic effects of IGIF, which possesses potent biologic activities, including the induction of IFN-gamma production by spleen cells and the enhancement of NK cell cytotoxicity.
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Interleukin-18 is a unique cytokine that stimulates both Th1 and Th2 responses depending on its cytokine milieu.

TL;DR: IL-18 should be seen as a unique cytokine that enhances innate immunity and both Th1- and Th2-driven immune responses and the expulsion of viruses is impaired in IL-18-deficient mice.