A recent experiment showed that in patients with acute myeloid leukemia, IDO-expressing tumor cells can induce the transformation of CD4+CD25-T cells to CD4+CD25+T cells [12]. In this study, we explored the inductive effect of IDO on Tregs isolated from the solid tumors of patients

with breast cancer, and used low expression of CD127 as a more accurate and specific surface molecular marker of inhibitory Tregs [9, 10]. We detected an increase in CD4+CD25+CD127- regulatory T cells in the CD3+T cell population from co-cultures of IDO-expressing CHO cells and CD3+T cells isolated from the peripheral blood of patients with FK228 concentration breast cancer. This phenomenon may be due to the IDO induced differentiation of CD3+T into CD4+CD25+CD127- cells, but further study will be needed to confirm this conclusion. Conclusions Endogenous E7080 cost IDO may be involved in a variety of peripheral CP673451 tolerance mechanisms and immunosuppressive responses, as well as having a role in other cellular mechanisms. We established a cell line that stably expressed IDO and preliminarily confirmed that active expression of IDO could

induce apoptosis in T cells isolated from the peripheral blood of patients with breast cancer; we confirm the role of IDO in the maturation and development of Tregs in breast cancer patients. This study provides an experimental basis for further study into the mechanism underlying the interaction between IDO and Tregs in tumor immunity. Ketotifen Acknowledgements We thanked Dr. Sharma’s work in establishment of the vivo model for activated mature Tregs by IDO. We also thanked Yizi Cong and Lijuan Wei of Tianjin Medical University Cancer Hospital and Institute for their technical assistance. This work was supported by grants from the National Natural Science Foundation of China (30972694, 81072159) and Tianjin Municipal Education Commission(20090133, 20090217), P. R. China. References

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