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      Interleukin (IL)-6 Directs the Differentiation of IL-4–producing CD4 + T Cells

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          Abstract

          Interleukin (IL)-4 is the most potent factor that causes naive CD4 + T cells to differentiate to the T helper cell (Th) 2 phenotype, while IL-12 and interferon γ trigger the differentiation of Th1 cells. However, the source of the initial polarizing IL-4 remains unclear. Here, we show that IL-6, probably secreted by antigen-presenting cells, is able to polarize naive CD4 + T cells to effector Th2 cells by inducing the initial production of IL-4 in CD4 + T cells. These results show that the nature of the cytokine (IL-12 or IL-6), which is produced by antigen-presenting cells in response to a particular pathogen, is a key factor in determining the nature of the immune response.

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          Most cited references42

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          Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction.

          A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described. The method provides a pure preparation of undegraded RNA in high yield and can be completed within 4 h. It is particularly useful for processing large numbers of samples and for isolation of RNA from minute quantities of cells or tissue samples.
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            IL-10 inhibits cytokine production by activated macrophages.

            IL-10 inhibits the ability of macrophage but not B cell APC to stimulate cytokine synthesis by Th1 T cell clones. In this study we have examined the direct effects of IL-10 on both macrophage cell lines and normal peritoneal macrophages. LPS (or LPS and IFN-gamma)-induced production of IL-1, IL-6, and TNF-alpha proteins was significantly inhibited by IL-10 in two macrophage cell lines. Furthermore, IL-10 appears to be a more potent inhibitor of monokine synthesis than IL-4 when added at similar concentrations. LPS or LPS- and IFN-gamma-induced expression of IL-1 alpha, IL-6, or TNF-alpha mRNA was also inhibited by IL-10 as shown by semiquantitative polymerase chain reaction or Northern blot analysis. Inhibition of LPS-induced IL-6 secretion by IL-10 was less marked in FACS-purified peritoneal macrophages than in the macrophage cell lines. However, IL-6 production by peritoneal macrophages was enhanced by addition of anti-IL-10 antibodies, implying the presence in these cultures of endogenous IL-10, which results in an intrinsic reduction of monokine synthesis after LPS activation. Consistent with this proposal, LPS-stimulated peritoneal macrophages were shown to directly produce IL-10 detectable by ELISA. Furthermore, IFN-gamma was found to enhance IL-6 production by LPS-stimulated peritoneal macrophages, and this could be explained by its suppression of IL-10 production by this same population of cells. In addition to its effects on monokine synthesis, IL-10 also induces a significant change in morphology in IFN-gamma-stimulated peritoneal macrophages. The potent action of IL-10 on the macrophage, particularly at the level of monokine production, supports an important role for this cytokine not only in the regulation of T cell responses but also in acute inflammatory responses.
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              Lymphocyte responses and cytokines.

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                Author and article information

                Journal
                J Exp Med
                The Journal of Experimental Medicine
                The Rockefeller University Press
                0022-1007
                1540-9538
                3 February 1997
                : 185
                : 3
                : 461-470
                Affiliations
                From the [* ]Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011; []Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-9031; and [§ ]Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520-8011
                Author notes

                Address correspondence to Dr. Richard A. Flavell, Section of Immunobiology, Yale University School of Medicine, PO Box 208011, New Haven, CT 06520-8011. M. Rincón's present address is the University of Vermont, Department of Medicine, Given Medical Bldg., Burlington, VT.

                Article
                10.1084/jem.185.3.461
                2196041
                9053446
                4ab9c007-dd62-4e1f-8d8d-00dc5a48befe
                Copyright @ 1997
                History
                : 30 October 1996
                : 21 November 1996
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                Medicine
                Medicine

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