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Role of T cells in granuloma formation induced by Rhodococcus aurantiacus is independent of their interferon-gamma production

Department of Microbiology, School of Medicine, Hokkaido University, Kita 15, Nishi 7, Kita-ku, Sapporo, Japan

Corresponding author: Dr Yimin.

Received 18 Dec. 2000; accepted 15 Feb. 2001.

Abstract

Intravenous injection of Rhodococcus aurantiacus into mice causes granulomatous inflammation dependent on endogenous interferon- (IFN-). This study investigated the mechanism of granuloma formation with an adoptive transfer system in IFN- knockout (IFN-^-/-) mice. IFN-^-/- 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-^+/+) mice did not restore granuloma formation, although this treatment diminished IL-10 production in IFN-^-/- mice. Adoptive transfer of splenocytes from infected IFN-^-/- mice into infected IFN-^+/+ reduced granuloma formation. These results suggest that splenocytes of IFN-^-/- mice suppress granuloma formation. On the other hand, although IFN- 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-^+/+ mice or IFN-^-/- mice could induce granuloma formation. This means that splenocytes of IFN-^-/- mice have the ability to both induce and suppress granuloma formation. Induction of granuloma is probably dependent on both T cells and IFN- produced by non-T cells. It is suggested that the role of T cells in granuloma formation is not dependent on their IFN- production.