Unregulated IL-23/IL-17 immune response in autoimmune diseases.
BACKGROUND
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 naïve 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.
Costa
Vinicius Silva
VS
Endocrinology Department, Medical Investigation Laboratory, 18-LIM-18, São Paulo University, São Paulo-SP, Brazil. vinicius.scosta@usp.br
Mattana
Teresa Cristina Colvara
TC
da Silva
Maria Elizabeth Rossi
ME
D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D006801:Humans; D007167:Immunotherapy; D020381:Interleukin-17 / Q000097:blood*; D053759:Interleukin-23 / Q000097:blood*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D020381:Interleukin-17; D053759:Interleukin-23