Journal
CANCER MEDICINE
Volume 9, Issue 15, Pages 5598-5608Publisher
WILEY
DOI: 10.1002/cam4.3213
Keywords
Epstein-Barr virus nuclear antigen 1; M2 macrophage; transforming growth factor beta 1; Treg
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Funding
- National Natural Science Foundation of China [81472535]
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Background Documented reports proved that Epstein-Barr virus (EBV) infection increased infiltration of Tregs in malignancy. However, the mechanism of EBV recruitment Tregs into nasopharyngeal carcinoma (NPC) tissues has not been detailed discussion. Methods Expression of EBV nuclear antigen 1 (EBNA1) and Foxp3 in NPC tissue samples was detected by immunohistochemistry. EBNA1+ NPC cell lines were used to coculture with PBMC, naive T cells, Tregs, and monocytes. Percent of Treg was detected by flow cytometry. Results EBNA1 protein was overexpressed in NPC tissues, and was associated with a number of infiltrated Tregs. EBNA1+ NPC cells converted naive T cells into Tregs by up-regulated TGF-beta 1. Enhanced CCL20 production in EBNA1-expressed tumor cells increased Tregs migration. Polarized-M2 macrophages by EBNA1 expression cells converted naive T cells into Tregs. Conclusions EBNA1 favors accumulation of Tregs in NPC through: (a) upregulated TGF-beta 1 converted naive T cell into Treg; (b) upregulated CCL20 increased Treg migration; and (c) polarized-M2 macrophage converted naive T cell into Treg.
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