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1 June 2003 Effects of 10-T Static Magnetic Field on Human Peripheral Blood Immune Cells
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Onodera, H., Jin, Z., Chida, S., Suzuki, Y., Tago, H. and Itoyama, Y. Effects of 10-T Static Magnetic Field on Human Peripheral Blood Immune Cells. Radiat. Res. 159, 775–779 (2003).

The exposure of peripheral blood mononuclear cells (PBMCs) was performed in a 10-T static magnetic field. Without lymphocyte stimulation, there were no significant differences in the viability of the exposed and unexposed CD4 T cells, CD8 T cells, B cells, and natural killer (NK) cells. The expression of Th1 type chemokine receptor, CXCR3, and Th2 type receptor, CCR3, was unaltered after magnetic-field exposure. No differences were observed in the naive T cells and memory T-cell subclasses in either CD4 or CD8 T cells. In contrast to the unstimulated condition, the magnetic-field exposure reduced the viability of phytohemagglutinin (PHA)-activated T cells in both the CD4 and CD8 subclasses. In particular, the number of PHA-treated naive CD8 T cells (CD45RA CD4CD8 ) was markedly decreased after the magnetic-field exposure, while PHA-treated memory CD8 cells (CD45RACD4CD8 ) were resistant to the exposure. The number of PHA-treated naive CD4 T cells (CD45RA CD4 CD8) and memory cells (CD45RACD4 CD8) was markedly decreased to a similar degree. Thus the susceptibility of lymphocytes to the magnetic-field exposure differed among activated T-cell subtypes. The magnetic-field exposure significantly increased the death of PHA-stimulated lymphocytes by apoptosis. These results suggest that a strong static magnetic field has acute effects on immune cells during cell division, while the field exposure has a minimal effect on immune cells in a nondividing phase.

Hiroshi Onodera, Zhe Jin, Susumu Chida, Yasushi Suzuki, Hideaki Tago, and Yasuto Itoyama "Effects of 10-T Static Magnetic Field on Human Peripheral Blood Immune Cells," Radiation Research 159(6), 775-779, (1 June 2003).[0775:EOTSMF]2.0.CO;2
Received: 24 June 2002; Accepted: 1 October 2002; Published: 1 June 2003

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