Immune cells are known to be vulnerable to radiation, through induced apoptosis (programmed cell death) in mature T and B lymphocytes (long-lived white blood cells responsible for adaptive immunity) and by lethal damage in bone marrow stem cell precursors of monocytes and granulocytes (short-lived white blood cells responsible for innate immunity) as well as natural killer cells (lymphocytes responsible for innate immunity).

In persons receiving heavy doses of A-bomb radiation, both mature lymphocytes and bone marrow stem cells were severely damaged, causing profound depletion of granulocytes and natural killer cells, which together defend against microbial (or bacterial and viral) invasion. As a result, many people died from active infections.

About two months after exposure, marrow stem cells recovered, and deaths due to infection generally ended. Studies of survivors since the 1980s have shown no abnormalities in monocytes, granulocytes, and natural killer cells, indicating that damage to innate immunity occurred only during the early period following the bombings.

The recovery of CD4 helper-T lymphocytes (a major subset of T lymphocytes responsible for antigen-specific immunity) took longer, and studies have shown that CD4 T lymphocytes recovered only incompletely. Even today, the relative number of CD4 T cells is, on average, 2% lower per Gy. More in-depth studies have shown that among those with higher radiation doses a greater proportion of T cells are “memory” T cells rather than newly formed naïve T cells, indicating reduced ability of the thymus to produce new T cells. In contrast to diminished CD4 T-cell numbers and function, the number of B cells is slightly higher in exposed persons, perhaps as a compensation. Tests show that CD4 T cells from high-dose persons tend to have less reactivity to an infectious agent. Also, as a compensation for decreased T-cell function, cells responsible for innate immunity are activated and produce inflammatory proteins, and our studies have shown that persons with higher radiation exposures have lower numbers of CD4 T cells and elevated levels of various inflammatory proteins in their blood. These trends parallel what is seen with advancing age, suggesting that radiation exposure may accelerate immune aging processes.

To date, there has been no clear evidence that any specific health effects have resulted from the persistent abnormalities observed in the T and B lymphocytes of A-bomb survivors. The reason may be that wide variations in specific immune responses make it difficult to identify persons with radiation-impaired immunity to specific pathogens. For example, in tuberculin testing for vaccination against tuberculosis, some people show immediate positive results, and others do not. There is also no evidence of radiation effects on risks for chronic infectious diseases, such as tuberculosis, or autoimmune diseases, such as rheumatoid arthritis. On the other hand, a slight dose-related decrease in immunity has been observed against certain viral infections. For example, the proportion of people who carry the hepatitis B virus increases by A-bomb dose.

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