Abstract

Decreased resistance to pathogens, which is an effect of ionizing radiations that is well documented in several animal species, is largely mediated by impairment of the specific immune response. The effects of irradiation on the antibody response have been extensively investigated during the past several decades. It has been established that the antibody response is depressed when the antigen is injected shortly before or immediately after irradiation. Recovery of the response in animals immunized after sublethal irradiation starts after about 1 week and may be complete 2 months after irradiation. If animals are immunized a few or several days before radiation exposure, some parameters of the antibody response are unaffected while others may display lower or higher values than normal, depending on the nature and physical form of the antigen. Recent studies have described the effects of whole-body irradiation on antibody affinity. Since this antibody property affects the stability of immune complexes and, therefore, the antibody's ability to neutralize viruses and toxins, affinity was felt to be of importance to counteract infections in irradiated animals. Antibody affiinity was found up to 20 times greater in irradiated than in control mice when antigen was injected 1–5 days before or 2 hr-8 weeks after a sublethal dose of X-rays. Recovery profiles of mitotic responses of spleen cells to PHA, ConA, or LPS suggest that the enhancement of antibody affinity in irradiated mice could result from a relative lack of suppressor T cells. Dysfunctions of the immune system of irradiated animals can be attributed to alterations of the populations of immunologically competent cells. Unlike auxiliary cells, lymphocytes are extremely sensitive to ionizing radiations. Subpopulations of T and B lymphocytes appear to have different radiosensitivities and to develop with different efficiencies in irradiated animals. B cells seem to be more radiosensitive and to recover faster than T cells. The radiosensitivity of lymphocytes decreases with differentiation from precursor to effector cells. However, like activated cytoxic cells, primed helper cells include very radiosensitive subpopulations.

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