In this paper we summarize the long-term effects of A-bomb radiation on the T-cell system and discuss the possible involvement of attenuated T-cell immunity in the disease development observed in A-bomb survivors. Our previous observations on such effects include impaired mitogen-dependent proliferation and IL-2 production, decreases in naive T-cell populations, and increased proportions of anergic and functionally weak memory CD4 T-cell subsets. In addition, we recently found a radiation dose-dependent increase in the percentages of CD25 /CD127− regulatory T cells in the CD4 T-cell population of the survivors. All these effects of radiation on T-cell immunity resemble effects of aging on the immune system, suggesting that ionizing radiation might direct the T-cell system toward a compromised phenotype and thereby might contribute to an enhanced immunosenescence. Furthermore, there are inverse, significant associations between plasma levels of inflammatory cytokines and the relative number of naïve CD4 T cells, also suggesting that the elevated levels of inflammatory markers found in A-bomb survivors can be ascribed in part to T-cell immunosenescence. We suggest that radiation-induced T-cell immunosenescence may result in activation of inflammatory responses and may be partly involved in the development of aging-associated and inflammation-related diseases frequently observed in A-bomb survivors.
How to translate text using browser tools
10 September 2010
T-Cell Immunosenescence and Inflammatory Response in Atomic Bomb Survivors
Yoichiro Kusunoki,
Mika Yamaoka,
Yoshiko Kubo,
Tomonori Hayashi,
Fumiyoshi Kasagi,
Evan B. Douple,
Kei Nakachi
ACCESS THE FULL ARTICLE
Radiation Research
Vol. 174 • No. 6b
December 2010
Vol. 174 • No. 6b
December 2010