Radiation Triggered Phenotypic Changes of Regulatory T Cells

Corresponding Author: Dongsheng Niu Department of Radiation Technology, Beijing Institute for Occupational Disease Prevention and Treatment, China Email: bzrp2021@163.com Abstract: Ionizing radiation disrupts the immune balance easily. Regulatory T (Treg) cells directly affect the immune balance after radiation exposure. Meanwhile, the present study is to investigate the survival ability and phenotypic changes of Treg cells induced by Co γ-rays in order to expand the understanding on how Treg cells modulated by radiation. Mice lymphocytes were isolated from thymus and spleen at 1, 4 and 10 days after 2 Gy Co γ-rays irradiation. The proliferation and phenotype of Treg cells were analyzed by flow cytometry. Helio Treg cells were calculated and ATP luminescence was measured by ELISA. CD39 from thymus and spleen was measured by flow cytometry. Moreover, miR-31 expression in the thymus and spleen post irradiation was determined by RT-PCR. The apoptosis rate of Treg cells was increased to 13.1% in thymus and 44.2% in the spleen after 2Gy irradiation. The proliferation of Treg cells in thymus decreased from 31.6 to 14.2% post irradiation (t = 3.56, 5.72, P<0.05). The percentage of Helio Treg cells increased and the mean florescence intensity of Helio in Treg cells increased from 5,677.7 to 6,529 in thymus and increased from 3,968.7 to 4,558.7 in spleen. The ratio of CD39 Treg in thymus was significantly increase from 43.2 to 83.8 after 10 days radiation (t = -18.29, P<0.05). ATP released by Treg cells was down-regulated after radiation (0.15 μmol/L, t = 31.98, p<0.05). Furthermore, miR-31 expression in CD4T cells significantly decreased after 2 Gy radiation in the thymus. This study indicating the relationship between radiation induced Treg cell apoptosis and phenotype changes in vivo and provided a theoretical basis for the prevention and treatment of radiation-induced immune imbalance. Our study offered a new idea for radiotherapy combined with immunotherapy by target-regulating CD39 and miR-31.