Retinoic acid (RA), which is the biologically active form of vitamin A, acts through the nuclear hormone receptor RAR (RA receptor) to induce either gene activation or repression. RA production and its effects have been linked to macrophages, dendritic cells, T and B cells, and iNKT cells in the immune system and play pro- as well as anti-inflammatory roles depending on the cell type and the immune context. In this issue of the European Journal of Immunology, Lee et al. [Eur. J. Immunol. 2012. 42: 1685-1694] show that RA ameliorates Con A-induced murine hepatitis by selectively downmodulating IFN-γ and IL-4 production in disease-causing NKT cells in the liver. Remarkably, this effect is restricted to this liver disease model and does not apply to αGalCer-induced murine liver injury, which is driven by other cytokines. The study identifies retinoid signaling as an important endogenous mechanism controlling immune reactions and also as a potential pharmacological target for treatment of hepatic liver injury. Furthermore, the study by Lee et al. provides additional support for the concept of metabolic regulation of immune function.
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