Project/Area Number |
16390190
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Public health/Health science
|
Research Institution | Radiation Effects Research Foundation |
Principal Investigator |
KUSUNOKI Yoichiro Radiation Effects Research Foundation, Department of Radiobiology/Molecular Epidemiology, Assistant Chief, 放射線生物学/分子疫学部, 副部長 (60333548)
|
Co-Investigator(Kenkyū-buntansha) |
HAYASHI Tomonori Radiation Effects Research Foundation, Department of Radiobiology/Molecular Epidemiology, Chief of Immunology Laboratory, 放射線生物学/分子疫学部, 免疫学研究室長 (70333549)
KYOIZUMI Seishi Yasuda Women's University, Department of Nutritional Sciences, Professor, 家政学部, 教授 (50333547)
HAKLODA Masayuki Yasuda Women's University, Department of Nutritional Sciences, Professor, 家政学部, 教授 (70208429)
|
Project Period (FY) |
2004 – 2006
|
Project Status |
Completed (Fiscal Year 2006)
|
Budget Amount *help |
¥14,300,000 (Direct Cost: ¥14,300,000)
Fiscal Year 2006: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2005: ¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 2004: ¥5,100,000 (Direct Cost: ¥5,100,000)
|
Keywords | Cohort study / Cellular immunity / Molecular epidemiology / Radiation / Cytokine / Virus hepatitis / Th1 / Th2 / 遺伝子多型 / 炎症 / CD4 |
Research Abstract |
To address whether immunogenetic background may determine individual susceptibility to disease among A-bomb survivors, we examined the relationships between cellular immunological parameters and polymorphisms of immune-related genes and analyzed their associations with disease development. The following results were obtained in this study period. 1.A radiation dose-dependent decrease in percentage of naive CD4 T cells in both Hiroshima and Nagasaki survivors; this is possibly due to radiation-induced suppression of CD4 T-cell production in the thymus. 2.Dose-dependent increases in percentages of the functionally weak and anergic subsets of memory CD4 T cells that were identified by CD43 expression level. 3.Dose-dependent increases in the levels of inflammatory cytokines (IL-6, IFN-γ, and TNF-α) in the blood. 4.Th1-dominant status associated with elevation of inflammatory cytokine levels in individuals with HCV infection as well as in progression of chronic hepatitis. 5.No significant phenotype-genotype association in inflammatory cytokine (IL-6, IFN-γ, and TNF-α) genes ; genotypes of these genes are unlikely to interact with radiation effects. 6.A suggestive association between CD45 exon 6 SNP (A138G) and proportion of Th1/Th2 cells. A follow-up study regarding disease development will be continued for the subjects in this study. Thus, this study provided not only evidence supporting our hypothesis that A-bomb irradiation has accelerated immunological aging but also a strong basis for further cohort study investigating relationships among radiation exposure, biological endpoints of cellular immunity, genetic backgrounds, and disease risks in a large human population.
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