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By Samuel Huber
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60] Santana G, Bendicho MT, Santana TC, Reis LB, Lemaire D, Lyra AC. The TNF-α -308 polymorphism may affect the severity of Crohn’s disease. Clinics (Sao Paulo). 2011; 66: 1373–1377. 43 44 New Insights into Inflammatory Bowel Disease [61] Maynard CL, Weaver CT. Diversity in the contribution of interleukin- 10 to T-cell-mediated immune regulation. Immunol Rev. 2008; 226: 219–233. [62] Thio CL. Host genetic factors and antiviral immune responses to hepatitis C virus. Clin Liver Dis. 2008; 12: 713–726.
The increased levels of IL-10 play a role in the amplification of humoral responses in some diseases [141]. Sanchez-Munoz et al. [143] suggested that the intestinal inflammation in IBD is controlled by a complex interplay of innate and adaptive immune mechanisms. Cytokines determine T-cell differentiation of Th1, Th2, T regulatory, and Th17 cells in IBD, and cytokines levels regulate the development, recurrence, and exacerbation of the inflammatory process in IBD. The dysregulation of T cells, or an over-production of effector T cells, results in the development and exacerbation of IBD [144].
Gut Liver. 2010; 4: 1–14. [17] Yun J, Xu CT, Pan BR. Epidemiology and gene markers of ulcerative colitis in the Chinese. World J Gastroenterol. 2009; 15: 788–803. [18] Waterman M, Xu W, Stempak JM, et al. Distinct and overlapping genetic loci in Crohn’s disease and ulcerative colitis: correlations with pathogenesis. Inflamm Bowel Dis. 2011; 17: 1936–1942. [19] Jump RL, Levine AD. Mechanisms of natural tolerance in the intestine: implications for inflammatory bowel disease. Inflamm Bowel Dis. 2004; 10(4): 462–478.