Unregulated IL-23/IL-17 immune response in autoimmune diseases

作者：Costa Vinicius Silva^*; Colvara Mattana Teresa Cristina; Rossi da Silva Maria Elizabeth

来源：Diabetes Research and Clinical Practice, 2010, 88(3): 222-226.

DOI：10.1016/j.diabres.2010.03.014

• Interleukin 23
• Autoimmunity
• Type 1 Diabetes

Introduction: Type 1A diabetes (T1D) is an autoimmune disease resulting from the selective destruction of pancreatic beta cells by T cells most likely due to interaction of environmental and genetic factors. The CD4((+)) T cells, largely implicated in this disease, comprise different subsets; based on the cytokines they produce. These subsets include Th1, Th2, regulatory T cells and another population of recently described T cells called Th17 cells. Increased expression of interleukin 17 (IL-17) has been detected in sera and in target tissues of patients with various autoimmune diseases. The differentiation of Th17 cells from naive T cells appears to involve signals from TGF-beta, IL-6, IL-21, IL-1beta and IL-23. IL-23, a member of the IL-12 family, which activate the effector function of Th17 cells to promote inflammatory responses. In animal models, IL-23 is involved in the development of autoimmune diabetes. In humans, it seems to cause multi-organ inflammation, contributing to rheumatoid arthritis, inflammatory bowel disease and celiac disease manifestations.
Conclusions: The discovery that certain autoimmune disorders might be largely mediated by an unregulated IL-23/IL-17 response has important implications for the development of novel therapies for these diseases.

• 出版日期2010-6