Augmentation of innate immunity by low-dose irradiation

Ren, Hongwei; Shen, Jiwei; Tomiyama-Miyaji, Chikako; Watanabe, Michitoshi; Kainuma, Eisuke; Inoue, Masashi; Kuwano, Yuh; Abo, Toru

doi:10.1016/j.cellimm.2007.02.009

Cited by 54 publications

(38 citation statements)

References 21 publications

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“…The anti-tumor effects of low-dose TBI could be explained at least partly by immune enhancement, induction of apoptosis in premalignant cells, and intrinsic hypersensitivity of certain cancer cell genotypes to low-dose radiation (19,20). Proposed mechanisms of immune enhancement include elimination of an especially radiosensitive subset of T-suppressor lymphocytes, increased secretion of cytokines that enhance cell-mediated responses, and expansion of extrathymic T, natural killer (NK) and NKT cells (21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

et al. 2012

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Health risks due to exposure to low-dose/low-dose-rate radiation alone or when combined with acute irradiation are not yet clearly defined. This study quantified the effects of protracted exposure to low-dose/low-dose-rate γ rays with and without acute exposure to protons on the response of immune and other cell populations. C57BL/6 mice were irradiated with ⁵⁷Co (0.05 Gy at 0.025 cGy/h); subsets were subsequently exposed to high-dose/high-dose-rate proton radiation (250 MeV; 2 or 3 Gy at 0.5 Gy/min). Analyses were performed at 4 and 17 days postexposure. Spleen and thymus masses relative to body mass were decreased on day 4 after proton irradiation with or without pre-exposure to γ rays; by day 17, however, the decrease was attenuated by the priming dose. Proton dose-dependent decreases, either with or without pre-exposure to γ rays, occurred in white blood cell, lymphocyte and granulocyte counts in blood but not in spleen. A similar pattern was found for lymphocyte subpopulations, including CD3+ T, CD19+ B, CD4+ T, CD8+ T and NK1.1+ natural killer (NK) cells. Spontaneous DNA synthesis by leukocytes after proton irradiation was high in blood on day 4 and high in spleen on day 17; priming with γ radiation attenuated the effect of 3 Gy in both body compartments. Some differences were also noted among groups in erythrocyte and thrombocyte characteristics. Analysis of splenocytes activated with anti-CD3/anti-CD28 antibodies showed changes in T-helper 1 (Th1) and Th2 cytokines. Overall, the data demonstrate that pre-exposure of an intact mammal to low-dose/low-dose-rate γ rays can attenuate the response to acute exposure to proton radiation with respect to at least some cell populations.

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Section: Introductionmentioning

confidence: 99%

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

et al. 2012

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“…It is well established that T cells transferred into such immunodeficient hosts will expand in a non-physiologic manner (homeostatic proliferation) that may result in artificial activation [23]. Moreover, irradiated hosts likely represent a highly inflammatory environment, ''hormesis effects'' [24]. Similarly, RAG-deficient mice have robust innate immune systems to partially compensate for the lack of adaptive immunity [25].…”

Section: Discussionmentioning

confidence: 99%

Involvement of CD8⁺ T cells in protective immunity against murine blood‐stage infection with Plasmodium yoelii 17XL strain

et al. 2010

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When developing malaria vaccines, the most crucial step is to elucidate the mechanisms involved in protective immunity against the parasites. We found that CD8+ T cells contribute to protective immunity against infection with blood‐stage parasites of Plasmodium yoelii. Infection of C57BL/6 mice with P. yoelii 17XL was lethal, while all mice infected with a low‐virulence strain of the parasite 17XNL acquired complete resistance against re‐infection with P. yoelii 17XL. However, the host mice transferred with CD8+ T cells from mice primed only with P. yoelii 17XNL failed to acquire protective immunity. On the other hand, the irradiated host mice were completely resistant to P. yoelii 17XL infection, showing no grade of parasitemia when adoptively transferred with CD8+ T cells from immune mice that survived infection with both P. yoelii XNL and, subsequently, P. yoelii 17XL. These protective CD8+ T cells from immune WT mice had the potential to generate IFN‐γ, perforin (PFN) and granzyme B. When mice deficient in IFN‐γ were used as donor mice for CD8+ T cells, protective immunity in the host mice was fully abrogated, and the immunity was profoundly attenuated in PFN‐deficient mice. Thus, CD8+ T cells producing IFN‐γ and PFN appear to be involved in protective immunity against infection with blood‐stage malaria.

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“…TBI also causes activation of antigen presenting cells, and can augment innate immunity and the anti-tumor function of adoptively transferred T cells directed to tumor antigens (9, 10). Recent studies have shown that the depletion of T cell subsets by TBI or total lymphoid irradiation (TLI) is not uniform, and is instead selective due to the differential sensitivity of the subsets to irradiation induced cell death(9, 11, 12). The selective depletion results in an altered balance of T cell subsets after non-myeloablative or myeloablative irradiation favoring regulatory T cells including CD4 + CD44 hi natural killer T (NKT) cells (9, 11).…”

Section: Introductionmentioning

confidence: 99%

Selective Resistance of CD44hi T Cells to p53-Dependent Cell Death Results in Persistence of Immunologic Memory after Total Body Irradiation

Yao

Jones

Kohrt

et al. 2011

The Journal of Immunology

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Our previous studies showed that treatment of mice with total body irradiation (TBI) or total lymphoid tissue irradiation (TLI) markedly changes the balance of residual T cell subsets to favor CD4+CD44hi natural killer T (NKT) cells due to differential resistance of the latter subset to cell death. The object of the current study was to further elucidate the changed balance and mechanisms of differential radioresistance of T cell subsets after graded doses of TBI. The experimental results show that CD4+ T cells were markedly more resistant than CD8+ T cells, and CD44hi T cells including NKT cells and memory T cells were markedly more resistant than CD44lo (naïve) T cells. The memory T cells immunized to alloantigens persisted even after myeloabloative (1,000cGy) TBI, and were able to prevent engraftment of bone marrow transplants. Although T cell death after 1,000cGy was prevented in p53−/− mice, there was progressive T cell death in p53−/− mice at higher doses. Whereas, p53 dependent T cell death changed the balance of subsets, the p53 independent T cell death did not. In conclusion, resistance of CD44hi T cells to p53 dependent cell death results in the persistence of immunological memory after TBI, and can explain the immune mediated rejection of marrow transplants in sensitized recipients.

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Augmentation of innate immunity by low-dose irradiation

Cited by 54 publications

References 21 publications

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

Involvement of CD8⁺ T cells in protective immunity against murine blood‐stage infection with Plasmodium yoelii 17XL strain

Selective Resistance of CD44hi T Cells to p53-Dependent Cell Death Results in Persistence of Immunologic Memory after Total Body Irradiation

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Augmentation of innate immunity by low-dose irradiation

Cited by 54 publications

References 21 publications

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

Low-Dose Total-Body γ Irradiation Modulates Immune Response to Acute Proton Radiation

Involvement of CD8+ T cells in protective immunity against murine blood‐stage infection with Plasmodium yoelii 17XL strain

Selective Resistance of CD44hi T Cells to p53-Dependent Cell Death Results in Persistence of Immunologic Memory after Total Body Irradiation

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Involvement of CD8⁺ T cells in protective immunity against murine blood‐stage infection with Plasmodium yoelii 17XL strain