Spleen contributes to restraint stress induced hepatocellular carcinoma progression.

Int Immunopharmacol

National & Local Joint Engineering Research Center of Biodiagnosis and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China; Department of Oncology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; Key Laboratory of Environment and Disease-Related Gene, Ministry of Education, Xi'an Jiaotong University, Xi'an, Shaanxi, China. Electronic address:

Published: June 2020

The spleen is the largest secondary immune organ and plays a critical role in the progression of tumor. Psychological stress promotes tumor progression through inhibiting antitumor immune. However, the role of spleen in tumor progression induced by stress is unclear. Here, we showed that restraint stress promoted tumor growth, increased the percentage of CD11bGr-1 MDSC while decreased the percentages of CD3NK1.1 NK and CD3NK1.1 NKT in the tumor tissues. Restraint stress decreased the percentages of CD3CD4 T lymphocytes and CD3CD8 T lymphocytes while increased the percentage of CD11bGr-1 MDSC in the blood of tumor-bearing mice. Restraint stress increased the percentages of CD3CD4 T lymphocytes, CD3CD8 T lymphocytes, CD4PD1 T lymphocytes and CD8PD1 T lymphocytes while decreased the percentage of CD11bGr-1 MDSC in the spleen of tumor-bearing mice. Interestingly, splenectomy inhibited tumor growth and attenuated the changes of CD3CD4 T lymphocytes, CD3CD8 T lymphocytes, and CD11bGr-1 MDSC in blood induced by chronic restraint stress. Finally, splenectomy blocked the increases of CD11bGr-1 MDSC but did not attenuate the decreases of CD3NK1.1 NK and CD3NK1.1 NKT in tumor tissue induced by chronic stress. Together, these data indicate that chronic restraint stress promotes hepatocellular carcinoma growth and suppresses the antitumor immunity of tumor-bearing mice. Splenectomy could inhibit tumor growth and partly block the decrease of antitumor immune activity induced by stress.

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http://dx.doi.org/10.1016/j.intimp.2020.106420DOI Listing

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