Journal of Clinical & Experimental Dermatology Research
Open Access
ISSN: 2155-9554
+44 1478 350008
ISSN: 2155-9554
+44 1478 350008
Crohn’s disease is an immune-mediated disorder. Tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) produced by Th1 lymphocytes have traditionally been shown to be important in the pathogenesis of Crohn’s disease. In addition, recent studies demonstrate more complex cytokine networks, in which Th17 cells play a central role. The expansion and maintenance of Th17 cell responses require the activity of interleukin-23 (IL-23), and thus IL-23/IL-17 axis has been suggested to play a major role in the pathogenesis of Crohn’s disease. Crohn’s disease presents with various mucocutaneous signs, some of which show similar histological features of non-caseating granulomas with multinucleated histiocytes. Specific mucocutaneous manifestations include metastatic (cutaneous) Crohn’s disease,
perianal fistula, and oral Crohn’s disease. Although not specific, other various manifestations which histologically show granulomatous conditions are sometimes associated with Crohn’s disease. Also, Crohn’s disease exhibits other organ manifestations such as joints, eyes, kidneys, liver and biliary tracts, and vasculature. Those disorders may share pathognomonic significance attributed to common or similar mechanisms. The efficacy of TNF-targeting therapies strongly suggests the pivotal role of TNF-α in Crohn’s disease. Anti-TNF therapies bring beneficial effects for not only intestinal, but also mucocutaneous, joint, and ocular involvements. In this review, recent insights of the pathogenesis of Crohn’s disease, as well as mucocutaneous manifestations associated with Crohn’s disease, are introduced.