Type III interferon-lambda (IFN-$\lambda$) plays a critical role against infection, particularly in mucosal infection in the respiratory and gastrointestinal tract. Our study and other previous studies have shown that porcine IFN-$\lambda$ more efficiently curtails the infection of porcine epidemic diarrhea virus (PEDV) in the intestine epithelia than type I IFN, whereas IFN-$\lambda$3 exerts a more potent effect than IFN-$\lambda$1. However, the underlying mechanism remains elusive, and in particular, the transcriptional profile induced by IFN-$\lambda$3 has not been reported. Here, to resolve the mechanism responsible for the disparity between IFN-$\lambda$3 and type I IFN in anti-mucosal virus infection, we compared the transcription profiles induced by the two IFNs in porcine intestinal epithelial (IPEC-J2) cells by RNA-Seq. Our results showed that the pretreatment of IPEC-J2 cells with IFN-$\lambda$3 resulted in the differential expression of 983 genes. In contrast, IFN-$\alpha$ only modified the expression of 134 genes, and 110 of these genes were also observed in the response to IFN-$\lambda$3. A transcriptional enrichment analysis indicated that IFN-$\lambda$3 or IFN-$\alpha$ regulates multiple cellular processes and that IFN-$\lambda$3 activates more robust signaling pathways, particularly the antiviral Jak-STAT signaling pathway, than IFN-$\alpha$. Furthermore, we verified the RNA-Seq results through an RT-qPCR analysis of IPEC-J2 cells and porcine enteroids. Moreover, transient expression of the porcine rsad2 and mx2 genes among the top 10 genes induced by IFN-$\lambda$3 significantly inhibited PEDV infection. Collectively, the data showed that IFN-$\lambda$3 induces a unique transcriptional profile that does not completely overlap with that induced by IFN-$\alpha$ and strongly elicits a set of genes responsible for the antiviral activity of IFN-$\lambda$3. These findings provide important knowledge regarding the elicited ISGs of type I and III IFNs in restricting porcine intestinal viral infection.