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IL-18 Stimulates the Proliferation and IFN- Release of CD4⁺ T Cells in the Chicken: Conservation of a Th1-Like System in a Nonmammalian Species¹

Thomas W. Göbel^*, Kirsten Schneider, Beatrice Schaerer^*, Iris Mejri^*, Florian Puehler, Steffen Weigend, Peter Staeheli and Bernd Kaspers^2,*

^* Institute for Animal Physiology, University of Munich, Munich, Germany; Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, University of Freiburg, Freiburg, Germany; and Institute for Animal Science, Mariensee, Federal Agricultural Research Center, Germany

The phylogeny of Th1 and Th2 subsets has not been characterized mainly due to the limited information regarding cytokines in nonmammalian vertebrates. In this study, we characterize a Th1-like regulatory system focusing on the IL-18-regulated IFN- secretion. Stimulation of splenocytes with chicken IL-18 induced high levels of IFN- secretion. Depletion of either macrophages or CD4⁺ T cells from the splenocyte cultures caused unresponsiveness to IL-18. In contrast, PBL were unresponsive to IL-18 in the presence or absence of macrophages, but IFN- secretion was stimulated by suboptimal anti-TCR cross-linking combined with IL-18. Splenocytes from five different chicken lines responded equally well to the IL-18 treatment. LSL chicken splenocytes, however, responded only to IL-18 when stimulated either with optimal TCR cross-linking alone or suboptimal TCR cross-linking combined with IL-18. IL-18 not only induced IFN- secretion, but also stimulated splenocyte proliferation. This IL-18-induced proliferation was compared with the effects observed with IL-2. Both cytokines activated the splenocytes as demonstrated by increased size and MHC class II Ag up-regulation in the case of IL-18. Phenotypic analyses following 6 days of culture revealed that IL-2 mainly affected the proliferation of CD8⁺ cells, whereas IL-18 had an opposite effect and stimulated the proliferation of CD4⁺ cells. Taken together, these results demonstrate the conservation of Th1-like proinflammatory responses in the chicken; they characterize IL-18 as a major growth factor of CD4⁺ T cells and identify two distinct mechanisms of IL-18-induced IFN- secretion.

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