Radiosensitivity of the immune response Humoral immunity

In general, radiation is more deleterious to the antibody response than to delayed hypersensitivity responses. In the primary antibody response, radiation suppresses the inductive more than the productive phase, because plasma cells, unlike immature B cells, are extremely radioresistant (D0 values of 60-90 Gy (6000-9000 rad)), and radiation does not affect the biological activity of antibodies. However, most plasma cells are short-lived and survive only for several days, resulting in the eventual reduction of antibody titers. Despite reduced antibody titers, the antibody affinity is considerably higher in irradiated animals than in nonirradiated animals, possibly due to the relatively greater radioresistance of more differentiated antibody-producing cells.

Radiation has been used as a tool to elucidate regulation of antibody production. Depending on the time of irradiation in relation to antigenic challenge, depression or augmentation in primary antibody response may result. For example, irradiation of mice with 4.4 Gy (440 rad), a few hours or days before antigen exposure, results in immune suppression, whereas the same dose of irradiation 4 days after antigenic challenge leads to enhanced titers of antibody. This may be based on selective radiosensitivity of certain suppressor cell populations. In addition to timing, the type of antigen, its mode of presentation, the animal species or strain, and the class of antibody are important in determining whether exposure to radiation will result in increased or decreased antibody titers.

Although the in vivo secondary response has repeatedly been found to be more radioresistant than the primary, the D0 values for immunoglobulin M (IgM) and IgG plaque-forming cells (PFCs) were found to be similar in the primary and secondary responses, and ranged from 0.8 to 1 Gy (80-100 rad). These findings indicate that factors other than B cell survival, operating in vivo, account for the relatively greater radioresistance of the secondary response. The mechanism of this enhanced radio-resistance may have a quantitative rather than qualitative basis.

Studies of mammalian T and B cells established that as far as death of dividing cells is concerned, the D0 for T and B cells is similar. Apoptotic death, however, is more rapid for B cells than T cells. The T helper cell is critical in determining the magnitude of the T-dependent antibody response to most common antigens. Although different experimental procedures have shown heterogeneity in the radiosensi-tivity of T helper cells, several conclusions can be drawn. Unprimed helper T cells are quite radiosensitive. Priming renders helper T cells resistant to several thousand rad. This resistance, however, can be demonstrated primarily in in vitro assays. In contrast, D0 values in in vivo adoptive transfer were found to be as low as 2.3 Gy (230 rad). These low D0 values were explained by the loss of homing capacity of irradiated lymphoid cells. Radioresistant primed T helper cells can survive and function until stimulated to divide, at which time mitotic death occurs.

Regulatory suppressor cells may also be divided into radiation-sensitive and radiation-resistant populations, with antigen or mitogen-activated suppressor cells being more radioresistant than resting cells.

Cellular immunity

Delayed-type hypersensitivity (DTH) is relatively radioresistant when compared to antibody production. However, as measurements of skin test reactions cannot be evaluated with the same degree of sensitivity as antibody titers, the D0 values for the DTH reactions are difficult to determine. The homing properties of the DTH subclass of T cells are impaired by radiation, similar to the T helper cells. Furthermore, irradiation of a recipient prior to cell transfer also results in reduced DTH.

The majority of cytotoxic T lymphocytes (CTLs) are radioresistant to doses of several thousands rad. However, a fraction of CTLs are sensitive to doses ranging from 2 to 5 Gy (200-500 rad). The radio resistant fraction of CTLs is particularly beneficial in resistance to those infections that depend on cell-mediated immunity, e.g. most viral infections.

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