Effects of n ‐3 PUFA on the CD 4 + type 2 helper T ‐cell‐mediated immune responses in F at‐1 mice

Scope It has been suggested that n ‐3 PUFA can be used as a preventive or therapeutic strategy to control allergic asthma. But little is known about the exact mechanisms by which n ‐3 PUFA modulates it. Here, the effects of elevated n ‐3 PUFA on ovalbumin ( OVA ) induced airway inflammation were investigated using F at‐1 transgenic mice that can convert n ‐6 PUFA to n ‐3 PUFA endogenously. Methods and results First, we tested whether F at‐1 expression modulates CD 4 + T‐cell activation, proliferation, and differentiation in vitro and found that the F at‐1 expression attenuated all of these CD 4 + T ‐cell responses by suppression of T ‐cell receptor mediated signaling and cytokine‐mediated phosphorylation of STAT s. When the F at‐1 mice were sensitized and challenged with the OVA , they showed a significant decrease in the recruitment of inflammatory cells into airway, the production of T h2 cytokines, eotaxin, and mucin in the lung, and the concentration of OVA ‐specific I g E in the serum. Furthermore, the differentiation of CD 4 + T cells into T h2 was also decreased in the spleen of F at‐1 mice. Conclusion Our results showed that an elevated level of n ‐3 PUFA was effective in preventing allergic airway inflammation by modulating the activation and differentiation of CD 4 + T cells in F at‐1 mice.