INTERLEUKIN-10 DOWN-REGULATES PROLIFERATION AND EXPRESSION OF INTERLEUKIN-2 RECEPTOR P55 CHAIN AND INTERFERON-GAMMA, BUT NOT INTERLEUKIN-2 OR INTERLEUKIN-4, BY PARASITE-SPECIFIC HELPER T-CELL CLONES OBTAINED FROM CATTLE CHRONICALLY INFECTED WITH BABESIA-BOVIS OR FASCIOLA-HEPATICA

Human recombinant interleukin-10 (IL-10) was previously shown to inhib it accessory cell (AC)-dependent proliferation of bovine parasite-spec ific T helper 1 (Th1), Th2, and Th0 cells in an IL-2-reversible manner (Brown, W.C., Woods, V.M., Chitko-McKown, C.G., Hash, S.M., and Rice- Ficht, A.C., 1994. Infect. Immun. 62, 4697-4708). The present study wa s therefore designed to determine whether the effect of IL-10 on T cel l proliferation corresponded with downregulated expression of cytokine s, or their receptors, important for T cell growth. The effects of IL- 10 on cellular proliferation and expression of IL-2, IL-4, IL-2 recept or (IL-2R; p55), and IFN-gamma by Babesia bovis- or Fasciola hepatica- specific Th cell clones were simultaneously evaluated. As shown previo usly, IL-10 strongly inhibited proliferation of all types of Th cell c lones, although this did not correspond with reduced expression of IL- 2 or IL-4 mRNA or their products. In contrast, expression of IL-2R mRN A was consistently reduced in the IL-10-treated clones. These results indicate that IL-10 does not inhibit AC-dependent proliferation of bov ine Th cells by downregulating T cell cytokines; rather, IL-10 may act by downregulating IL-2R p55 expression and subsequent signal transduc tion leading to decreased cellular proliferation. IFN-gamma production was also consistently downregulated in the presence of IL-10.