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1 October 2008 Repeated 0.5-Gy γ Irradiation Attenuates Experimental Autoimmune Encephalomyelitis with Up-regulation of Regulatory T Cells and Suppression of IL17 Production
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Abstract

Tsukimoto, M., Nakatsukasa, H., Sugawara, K., Yamashita, K. and Kojima, S. Repeated 0.5-Gy γ Irradiation Attenuates Experimental Autoimmune Encephalomyelitis with Up-regulation of Regulatory T Cells and Suppression of IL17 Production. Radiat. Res. 170, 429–436 (2008).

We recently reported attenuation of autoimmune disease by low-dose γ irradiation (repeated doses of 0.5 Gy) in MRL-lpr/ lpr mice. Here we studied the effect of low-dose γ irradiation on experimental autoimmune encephalomyelitis (EAE), which is a rodent model of multiple sclerosis. SJL/J mice were immunized with myelin basic protein for the induction of EAE and were exposed to 0.5 Gy γ rays once a week for 4 weeks. Radiation suppressed incidence and disease severity scores and delayed the onset of pathological changes. Pro-inflammatory cytokines (IFN-γ and IL6), autoantibody and CD8 cytotoxic T cells are involved in the appearance of EAE. Radiation suppressed the increases in these cytokines and the autoantibody production and blocked the increase in the population of CD8 cytotoxic T cells. Production of IL17 by Th17 cells and/or γδ T cells, which plays a crucial role in EAE, was also significantly suppressed by radiation. Furthermore, a significant increase in regulatory T cells, which are involved in suppression of autoimmune disease, was found in irradiated EAE mice. These data suggest that low-dose γ irradiation attenuates EAE through suppression of pro-inflammatory cytokines, reduction of cytotoxic T cells and induction of regulatory T cells.

Mitsutoshi Tsukimoto, Hiroko Nakatsukasa, Keigo Sugawara, Keiichiro Yamashita, and Shuji Kojima "Repeated 0.5-Gy γ Irradiation Attenuates Experimental Autoimmune Encephalomyelitis with Up-regulation of Regulatory T Cells and Suppression of IL17 Production," Radiation Research 170(4), 429-436, (1 October 2008). https://doi.org/10.1667/RR1352.1
Received: 25 January 2008; Accepted: 1 June 2008; Published: 1 October 2008
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