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         headline:Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain
         description:Interleukin-12 (IL-12) is a heterodimeric molecule composed of p35 and p40 subunits. Analyses in vitro have defined IL-12 as an important factor for the differentiation of naive T cells into T-helper type 1 CD4+ lymphocytes secreting interferon-γ (refs 1, 2). Similarly, numerous studies3,4,5,6,7 have concluded that IL-12 is essential for T-cell-dependent immune and inflammatory responses in vivo, primarily through the use of IL-12 p40 gene-targeted mice and neutralizing antibodies against p40. The cytokine IL-23, which comprises the p40 subunit of IL-12 but a different p19 subunit8, is produced predominantly by macrophages and dendritic cells, and shows activity on memory T cells. Evidence from studies of IL-23 receptor expression9 and IL-23 overexpression in transgenic mice10 suggest, however, that IL-23 may also affect macrophage function directly. Here we show, by using gene-targeted mice lacking only IL-23 and cytokine replacement studies, that the perceived central role for IL-12 in autoimmune inflammation, specifically in the brain, has been misinterpreted and that IL-23, and not IL-12, is the critical factor in this response. In addition, we show that IL-23, unlike IL-12, acts more broadly as an end-stage effector cytokine through direct actions on macrophages.
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      description:Interleukin-12 (IL-12) is a heterodimeric molecule composed of p35 and p40 subunits. Analyses in vitro have defined IL-12 as an important factor for the differentiation of naive T cells into T-helper type 1 CD4+ lymphocytes secreting interferon-γ (refs 1, 2). Similarly, numerous studies3,4,5,6,7 have concluded that IL-12 is essential for T-cell-dependent immune and inflammatory responses in vivo, primarily through the use of IL-12 p40 gene-targeted mice and neutralizing antibodies against p40. The cytokine IL-23, which comprises the p40 subunit of IL-12 but a different p19 subunit8, is produced predominantly by macrophages and dendritic cells, and shows activity on memory T cells. Evidence from studies of IL-23 receptor expression9 and IL-23 overexpression in transgenic mice10 suggest, however, that IL-23 may also affect macrophage function directly. Here we show, by using gene-targeted mice lacking only IL-23 and cytokine replacement studies, that the perceived central role for IL-12 in autoimmune inflammation, specifically in the brain, has been misinterpreted and that IL-23, and not IL-12, is the critical factor in this response. In addition, we show that IL-23, unlike IL-12, acts more broadly as an end-stage effector cytokine through direct actions on macrophages.
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      name:Department of Immunology, DNAX Research Inc., Palo Alto, USA
      name:Department of Immunology, DNAX Research Inc., Palo Alto, USA
      name:Department of Immunology, DNAX Research Inc., Palo Alto, USA
      name:Department of Protein and Antibody Technology, DNAX Research Inc., Palo Alto, USA
      name:Department of Protein and Antibody Technology, DNAX Research Inc., Palo Alto, USA
      name:Department of Protein and Antibody Technology, DNAX Research Inc., Palo Alto, USA
      name:Department of Protein and Antibody Technology, DNAX Research Inc., Palo Alto, USA
      name:Department of Immunology, Schering-Plough Research Institute, Kenilworth, USA
      name:Department of Immunology, Schering-Plough Research Institute, Kenilworth, USA
      name:Immunobiology Center, Mount Sinai School of Medicine, New York, USA
      name:Department of Genomics, DNAX Research Inc., Palo Alto, USA
      name:Department of Genomics, DNAX Research Inc., Palo Alto, USA
      name:Department of Immunology, DNAX Research Inc., Palo Alto, USA
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