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Long chain fatty acids (LCFAs) exert pro-inflammatory effects  in vivo . However, little is known regarding the effect of LCFAs on invariant ( i ) NKT cell functions. Here, we report an inhibitory effect of saturated LCFAs on transcription factors in  i NKT cells. Among the saturated LCFAs, palmitic acid (PA) specifically inhibited IL-4 and IFN-γ production and reduced  gata-3  and  t-bet  transcript levels in  i NKT cells during TCR-mediated activation. In  i NKT cells, PA was localized and induced dilation in the endoplasmic reticulum and increased the mRNA levels of downstream molecules of IRE1α RNase. Moreover, PA increased the degradation rates of  gata-3  and  t-bet  mRNA, which was restored by IRE1α inhibition or transfection with mutant  gata-3  or  t-bet , indicating that  gata-3  and  t-bet  are cleaved via regulated IRE1α-dependent decay (RIDD). A PA-rich diet and PA injection suppressed IL-4 and IFN-γ production by  i NKT cells in C57BL/6, but not Jα18 knockout mice, which was restored by injection of STF083010, an IRE1α-specific inhibitor. Furthermore, a PA-rich diet and PA injection attenuated arthritis in an  i NKT cell-dependent manner. Taken together, our experiments demonstrate that a saturated LCFA induced RIDD-mediated  t-bet  and  gata-3  mRNA degradation in  i NKT cells, thereby suppressing arthritis.

Palmitate inhibits arthritis by inducing t-bet and gata-3 mRNA degradation in iNKT cells via IRE1α-dependent decay