The type and magnitude of specific immune responses is determined by the interaction of antigen-presenting cells such as dendritic cells and macrophages with T and B lymphocytes. However, the effector arms of the immune system depend on interactions of numerous leukocyte subsets. In addition to lymphocytes and macrophages, natural killer
(NK) cells, eosinophils and granulocytes contribute significantly to host resistance to infections.
Macrophages are relatively radioresistant, as are other nondividing cells in the body. Although phagocytic function and migratory activity of the macrophage are resistant to doses of up to 100 Gy (10 000 rad) given to cells in vitro, it is uncertain whether at these doses macrophages maintain their ability to catabolize, degrade, produce antigenic peptides or kill microbial organisms. In general, macrophages are activated following irradiation, as evidenced by enhanced RNA synthesis, enhanced production of cytokines such as IL-1, and increased production and release of lysosomal enzymes.
As in the case of macrophages, the phagocytic ability of polymorphonuclear cells (PMNs) is not decreased by radiation. Moreover, radiation given during or following phagocytosis increases the intracellular killing capacity of these cells. However, radiation results in profound depression of PMN production, due to the destruction of extremely radiosensitive progenitors (D0, the dose of radiation that reduces survival of cells to 37% on the exponential portion of the survival curve, is only
0.9 Gy (90 rad) in mice). Given the short lifespan of mature PMNs, a dose of a few gray (a few hundred rads) leads to greatly reduced numbers of PMNs in the circulation within days after irradiation and results in enhanced susceptibility to infections.
Lymphocytes are unique in that the majority of mature resting lymphocytes die rapidly, within hours, after low doses (0.8-5 Gy (80-500 rad)) of radiation. Lymphocytes stimulated by antigen or mitogen, however, become much more radioresistant and maintain their function and viability even after relatively high doses (e.g. 10 Gy (1000 rad)) of radiation (Table 1). The exact mechanism for such enhanced radioresistance remains unknown, but may be based on altered pathways leading to apoptotosis,
1.e. reduced expression of p53 and/or increased expression of apoptosis-preventing molecules, such as Bcl-2. Alternatively, because mitogen-stimulated lymphocytes contain elevated levels of DNA polymerase and ligase it has been suggested that these cells have an enhanced ability to repair single-strand scissions in DNA.
Table 1 Radiosensitivity of cellular components of the immune system
Type of cell
Macrophages B cells Plasma cells T helper cells T suppressor cells T cytotoxic cells Granulocytes Natural killer cells Hematopoietic precursors
Unprimed 1-2 Gy (100-200 rad) Unprimed 1-5 Gy (100-500 rad) Minority 2-5 Gy (200-500 rad)
Resistant to in vitro doses of 100 Gy (10 000 rad)
60-90 Gy (6000-9000 rad)
Resistant to -50 Gy (several thousand rad)
Resistant to 20 Gy (2000 rad)
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