Crohn’s disease (CD) is a chronic inflammatory condition that can affect different portions of the gastrointestinal tract. Lymphatic drainage was demonstrated to be dysfunctional in CD pathogenesis, ultimately causing the failure of the resolution of intestinal inflammation. To investigate the molecular mechanisms underlying these dysfunctions, we isolated human intestinal lymphatic endothelial cells (HILEC) from surgical specimens collected from patients with CD (CD HILEC) and from healthy gut tissues (Healthy HILEC). Both cell types underwent transcriptomic profiling, and their barrier functionality was tested using a transwell-based coculture system between HILEC and lamina propria mononuclear cells (LPMCs). Results show CD HILEC to display a peculiar transcriptomic signature, that highlights mTOR signaling as an orchestrator of leukocyte trafficking through the lymphatic barrier of CD patients. Moreover, we demonstrate that LPMC transmigration through the lymphatic endothelium of patients with CD depends on the capability of mTOR to trigger the Interleukin 20 receptor subunit α (IL20RA)-mediated intracellular signaling. Conclusively, our study suggests that the leukocyte trafficking through the intestinal lymphatic microvasculature can be controlled by modulating IL20RA, thus leading to the resolution of chronic inflammation in patients with CD.