Th1-derived cytokine IFN-gamma is a potent inhibitor of eotaxin synthesis in vitro.

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Abstract
Eotaxin potentially plays an integral role in tissue eosinophilia. Inasmuch as Th2-derived cytokine IL-4 has been shown to stimulate eotaxin generation, we investigated here the effect of Th1-derived cytokine IFN-γ on human eotaxin production. IFN-γ but not -α or -β potently inhibited tumor necrosis factor (TNF)-α-induced eotaxin generation by dermal fibroblasts. The inhibitory effect was unique to eotaxin, because production of IL-8 or monocyte chemoattractant protein (MCP)-1 protein was not affected by the treatment with IFN-γ. Furthermore, the suppressive effect of IFN-γ was not cell-type or stimulus specific. The level of eotaxin mRNA increased within 2 h after activation with TNF-α and continued to increase up to 72 h. IFN-γ did not inhibit, but rather augmented the TNF-α-induced accumulation of mRNA in the early phase (~6 h). However, in the later phase, IFN-γ completely prevented the subsequent elevation of eotaxin mRNA and sustained it at low levels. Although the protective effect of IFN-γ against allergic inflammation has been assumed to result from its sole regulation of the proliferation of Th2-type T lymphocytes, these results imply that IFN-γ can also directly act on stromal cells to inhibit eotaxin production and consequently intervene in eosinophil recruitment.

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