Retinoic acid alleviates C on A ‐induced hepatitis and differentially regulates effector production in NKT cells

Retinoic acid ( RA ) is a diverse regulator of immune responses. Although RA promotes natural killer T ( NKT ) cell activation in vitro by increasing CD 1d expression on antigen‐presenting cells ( APC s), the direct effects of RA on NKT ‐cell responses in vivo are not known. In the present study, we...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:European journal of immunology 2012-07, Vol.42 (7), p.1685-1694
Hauptverfasser: Lee, Kyoo‐A, Song, You Chan, Kim, Ga‐Young, Choi, Gyeyoung, Lee, Yoon‐Sook, Lee, Jung‐Mi, Kang, Chang‐Yuil
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Retinoic acid ( RA ) is a diverse regulator of immune responses. Although RA promotes natural killer T ( NKT ) cell activation in vitro by increasing CD 1d expression on antigen‐presenting cells ( APC s), the direct effects of RA on NKT ‐cell responses in vivo are not known. In the present study, we demonstrated the effect of RA on the severity of C on A ‐induced hepatitis and molecular changes of NKT cells. First, we demonstrated that C on A ‐induced liver damage was ameliorated by RA . In correlation with cytokine levels in serum, RA regulated the production of IFN ‐γ and IL ‐4 but not TNF ‐α by NKT cells without influencing the NKT ‐cell activation status. However, RA did not alleviate α‐ G al C er‐induced liver injury, even though it reduced IFN ‐γ and IL ‐4 but not TNF ‐α levels in serum. This regulation was also detected when liver mononuclear cells ( MNC s) or NKT hybridoma cells were treated with RA in vitro. The regulatory effect of RA on NKT cells was mediated by RAR ‐α, and RA reduced the phosphorylation of MAPK . These results suggest that RA differentially modulates the production of effector cytokines by NKT cells in hepatitis, and the suppressive effect of RA on hepatitis varies with the pathogenic mechanism of liver injury.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.201142322