CD103+ Dendritic Cell Function Is Altered in the Colons of Patients with Ulcerative Colitis

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Human intestinal innate myeloid cells can be divided into 3 subsets: HLA-DRhighCD14+ cells, HLA-DRhighCD103+ dendritic cells (DCs), and HLA-DRhighCD14−CD103− cells. CD103+ DCs generate Treg cells and Th17 cells in the ileum, but their function in the colon remains largely unknown. This study characterized CD103+ DCs in the colon and investigated whether these cells are implicated in the pathogenesis of ulcerative colitis (UC).


Normal intestinal mucosa was obtained from intact sites of patients with colorectal cancer (n = 24). Noninflamed and inflamed colonic tissues were obtained from surgically resected specimens of patients with UC (n = 13). Among Lin−CD45+HLA-DRhigh intestinal lamina propria cells, CD14+ cells and CD103+ DCs were sorted and analyzed for microRNA expression of cytokines and toll-like receptors by quantitative real-time polymerase chain reaction. In addition, IL-4/IL-5/IL-13/IL-17/IFN-γ production and Foxp3 expression by naive T cells cultured with CD14+ cells and CD103+ DCs were analyzed.


CD103+ DCs in the normal colon showed lower expression of toll-like receptors and proinflammatory cytokines than CD14+ cells. Coculture with naive T cells revealed that CD103+ DCs generated Treg cells. CD103+ DCs from patients with UC did not generate Treg cells, but they induced IFN-γ-, IL-13-, and IL-17-producing CD4+ T cells and showed higher expression of IL6 (P < 0.0001), IL23A (P < 0.05), IL12p35 (P < 0.05), and TNF (P < 0.05).


In patients with UC, CD103+ DCs show the impaired ability to generate Treg cells, but exhibit a colitogenic function inducing Th1/Th2/Th17 responses. These findings show how human CD103+ DCs could contribute to the pathogenesis of UC.

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