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It is now well documented that the mode of primary stimulation in the mouse determines the ratio of Th1-, Th0- or Th2-type T cells obtained. In this paper we determine whether driving and cloning human peripheral blood mononuclear cells (PBMC) non-specifically with interleukin-2 (IL-2) and/ or IL-4 and mitogen, will differentially select T cells for IL-10 production. The presence of IL-2 during culture (with or without IL-4) yielded predominantly Th1-type clones (81% of clones with IL-2 alone and 77% with IL-2 + IL-4) and a low frequency of Th0-type clones (19% of clones with IL-2 and 10% of clones with IL-2 + IL-4), whereas IL-4 alone increased the yield of the IL-4 producing Th0 (35%) clones. The proportions of IL-2-producing clones did not alter with treatment; however, the combination of IL-2 + IL-4 altered the proportions of IL-10-producing clones. 47% of IL-2-cultured cells and 51% of IL-4-cultured cells produced IL-10 respectively, whereas only 22% of clones driven with IL-2 + IL-4 produced detectable levels of IL-10. Thus in the preliminary experiments described here we have demonstrated that the cytokines used to initially drive out human T cells and maintain the T-cell growth can skew the Th1/Th2/Th0 cytokine profiles of the clones obtained from mitogen-stimulated cultures. Moreover and unexpectedly the proportion of IL-10-producing cells is altered. These results are important in interpreting analysis of the cytokine profiles of human T cells and raise questions concerning how we should derive T-cell clones for a cytokine analysis that truly reflects the in vivo situation. [ABSTRACT FROM AUTHOR]

Results of in vivo and in vitro experiments suggest that the early suppression of brucella growth in double stranded polyadenylic-polyuridylic acid(poly A: U-) treated mice was due to a non-specific activation of macrophages by poly A: U. Poly A: U administered intraperitoneally at the time of brucella infection failed to enhance T-cell mediated responses to the organism, namely delayed-type hypersensitivity to brucellin and adoptive transfer of immunity to the infection. Poly A: U did not augment the protective antibodies formed in response to infection. Although poly A:U has been previously found to suppress brucellosis in athymic (nude) mice, it did not enhance the thymus-dependent antibody response to sheep erythrocytes in brucella-infected nudes, suggesting that it did not significantly enhance maturation of their helper T-cell percursors. Increased macrophage spreading, an indication of activation, was seen immediately after administration of poly A: U and Brucella abortus. Later on the infection spreading was suppressed, a phenomenon which appears to relate to the biphasic effect of poly A: U in vivo described in the accompanying paper. Peritoneal macrophages treated in vitro with poly A: U were stimulated to spread on plastic surfaces, even when T lymphocytes were removed with anti-Thy-1 serum and complement. [ABSTRACT FROM AUTHOR]