Epidemiological data assessing the role of TLR2 in the pathogenesis of IBD are scarce; nevertheless, monocytes isolated from patients with active IBD had higher expression levels of TLR2 on their cell surfaces and a significantly increased TNF-α production in response to TLR2 agonist stimulation as compared to inactive patients and healthy controls [61,62]. Here, TNF is linked to inflammatory bowel disease.