NDLI: Decreased indoleamine 2,3-dioxygenase expression in dendritic cells and role of indoleamine 2,3-dioxygenase-expressing dendritic cells in immune thrombocytopenia

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Decreased indoleamine 2,3-dioxygenase expression in dendritic cells and role of indoleamine 2,3-dioxygenase-expressing dendritic cells in immune thrombocytopenia

Content Provider	Semantic Scholar
Author	Xu, Shu-Qian Wang, Chun-Yan Zhu, Xiao-Juan Dong, Xiao-Yuan Peng, Jun Qin, Ping Sun, Jian-Zhi Guo, Cheng-Shan Ni, Heyu Hou, Ming
Copyright Year	2012
Abstract	Indoleamine 2,3-dioxygenase (IDO) expression in dendritic cells (DCs) can induce or maintain peripheral immune tolerance. Impaired IDO-mediated tryptophan catabolism has been observed in autoimmune diseases. In order to investigate the effects of IDO-mediated tryptophan catabolism and IDO-expressing DCs in immune thrombocytopenia, the concentrations of kynurenine were detected by high-pressure liquid chromatography. The expressions of IDO were analyzed by flow cytometry and western blot analysis. The effects of IDO+ DCs stimulated with CTLA-4-Ig on T cells proliferation and activation, lymphocyte apoptosis, and Tregs were measured by flow cytometry. We found that the expression of IDO in DCs of immune thrombocytopenia (ITP) patients was significantly decreased. CTLA-4-Ig significantly increased the expression of functional IDO in DCs of ITP patients. IDO+ DCs stimulated with CTLA-4-Ig suppressed T cells proliferation and activation, promoted lymphocyte apoptosis, and increased the percentage of Tregs. These results suggest that decreased IDO expression in DCs may play a critical role in ITP. CTLA-4-Ig successfully corrected the disorder of IDO expression in ITP. IDO+ DCs stimulated with CTLA-4-Ig inhibited immune responses by an IDO-dependent mechanism. Increasing the expression and activity of IDO in DCs might be a promising therapeutic approach for ITP.
Starting Page	1623
Ending Page	1631
Page Count	9
File Format	PDF HTM / HTML
DOI	10.1007/s00277-012-1451-0
PubMed reference number	22526360
Journal	Medline
Volume Number	91
Alternate Webpage(s)	http://or.nsfc.gov.cn/bitstream/00001903-5/126169/1/1000003927888.pdf
Journal	Annals of Hematology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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