TY - JOUR
T1 - Would eating carrots protect your liver? A new role involving NKT cells for retinoic acid in hepatitis
AU - Nagy, Laszlo
N1 - Copyright:
Copyright 2013 Elsevier B.V., All rights reserved.
PY - 2012/7
Y1 - 2012/7
N2 - 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. [] 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.
AB - 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. [] 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.
KW - Hepatitis
KW - NKT cells
KW - RAR
KW - Retinoids
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U2 - 10.1002/eji.201242705
DO - 10.1002/eji.201242705
M3 - Comment/debate
C2 - 22806070
AN - SCOPUS:84864021598
VL - 42
SP - 1677
EP - 1680
JO - European Journal of Immunology
JF - European Journal of Immunology
SN - 0014-2980
IS - 7
ER -