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Intravenous injection of Rhodococcus aurantiacus into mice causes granulomatous inflammation dependent on endogenous interferon-γ (IFN-γ). This study investigated the mechanism of granuloma formation with an adoptive transfer system in IFN-γ knockout (IFN-γ−/−) mice. IFN-γ−/− mice infected with R. aurantiacus did not develop granulomas, and high titres of endogenous interleukin-10 (IL-10) were detected in spleen extracts at 2 weeks after infection. The adoptive transfer of splenocytes from infected wild-type (IFN-γ+/+) mice did not restore granuloma formation, although this treatment diminished IL-10 production in IFN-γ−/− mice. Adoptive transfer of splenocytes from infected IFN-γ−/− mice into infected IFN-γ+/+ reduced granuloma formation. These results suggest that splenocytes of IFN-γ−/− mice suppress granuloma formation. On the other hand, although IFN-γ production induced by R. aurantiacus infection was detected in nude mice, which are deficient in T cells, granuloma formation was not induced in them. However, adoptive transfer of immune splenocytes from either IFN-γ+/+ mice or IFN-γ−/− mice could induce granuloma formation. This means that splenocytes of IFN-γ−/− mice have the ability to both induce and suppress granuloma formation. Induction of granuloma is probably dependent on both T cells and IFN-γ produced by non-T cells. It is suggested that the role of T cells in granuloma formation is not dependent on their IFN-γ production.