Purpose: Ionizing radiation is known to reduce the helper T (Th) 1 like function, resulting in a Th1/Th2 imbalance. We studied whether NK1.1+T cells which were the most resistant against gamma-irradiation impact on the imbalanced immune response after irradiation.
Materials and methods: C57BL/6 mice received a whole-body gamma-irradiation (WBI) of 4 Gy. The primary T cells were separated by magnetic cell sorter (MACS) using the anti-CD90.2 antibody. The apoptotic cells were detected by propidium iodide (PI) staining. To determine the Th1 and Th2 cell functions, the production of interferon (IFN)-gamma and interleukin (IL)-4 were analysed by a reverse transcriptase-polymerase chain reaction (RT-PCR) and an enzyme linked immunosorbent assay (ELISA). NK1.1+T cells were detected by flow cytometry. For depletion of the NK1.1+T cells in the WBI mice, anti-asialo GM1 antiserum was injected.
Results: The CD90.2 positive cells of the WBI mice produced significantly more Th2 type cytokines and also produced Th1 type cytokines at a not lower level than normal mice, and contained a higher absolute number of NK1.1+T cells. Also, the proportion of the NK1.1+T cells increased in the WBI mice. We found that the NK1.1+T cells were resistant to radiation-induced apoptosis in comparison with the conventional T cells. The depletion of NK1.1+T cells in WBI mice resulted in higher production of IgE and IL-4 and lower secretion of IL-12p70.
Conclusion: Our findings revealed that NK1.1+T cells that survive at an early stage after irradiation play an important role in the balance of the immune responses at a late stage after irradiation.