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Results for “RADIATION IMMUNOLOGY”

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At least 19 recordsLinked to original sources
PubMed1984

Immunological unresponsiveness induced by ultraviolet radiation.

Immunological unresponsiveness can be initiated by exposure of mice to UV radiation, followed by the introduction of certain antigens. These antigens include epicutaneously applied chemicals that induce contact hypersensitivity (CHS), and antigens that occur on skin cancers induced by UV radiation. Mice exposed repeatedly to high doses of UV radiation during UV carcinogenesis develop immunological unresponsiveness to UV radiation-induced skin cancers, which are highly antigenic. This unresponsiveness is associated with the appearance of suppressor T lymphocytes that are specific for tumors induced by UV radiation, even though these tumors express individually specific transplantation rejection antigens. Thus, the occurrence of suppressor cells with specificity for a set of non-cross-reacting tumors suggests that a common, UV-associated regulatory antigen or determinant may be present on UV-induced skin cancers. Suppression of CHS in mice by UV radiation can be induced by two different procedures. One involves applying the sensitizer directly on skin exposed to low doses of UV-B radiation and is thought to result from a direct effect of UV radiation on cutaneous Langerhans cells. The second involves application of the sensitizer to the unirradiated skin of mice or guinea pigs exposed several days earlier to a higher dose of UV-B radiation. The mechanism of the latter phenomenon is not well understood, but there is evidence that it results from an alteration of antigen presentation by splenic macrophages. Both forms of suppression are associated with the appearance of antigen-specific suppressor lymphocytes in the animals' spleens, which prevent the induction of CHS upon transfer to a normal recipient. Either or both of these pathways could be responsible for the formation of the suppressor cells involved in UV carcinogenesis. Recent studies suggest that UV radiation may also affect immunological responsiveness in humans as well as in animals. However, the extent of such alterations and the mechanisms by which they occur are still unknown.

Animals↗
PubMed1994

Ultraviolet radiation and immunology: something new under the sun--presidential address.

The carcinogenic activity of solar radiation has been known for nearly a century. However, within the past few years, we have realized that exposing the skin to sunlight also has profound immunological effects on the host and that these immunological changes can contribute to the development of skin cancer and alter host resistance to infectious diseases. These findings have led to the development of a new field of research, termed photoimmunology, which is concerned with the effects of UV radiation on immunological processes. Our interest in this field arose from studies on the antigenic properties of skin cancers induced in mice by chronic exposure to UV-B (280-320 nm) radiation. These cancers are highly antigenic and many are immunologically rejected upon transplantation to normal syngeneic recipients. In studying how these cancers were able to survive and grow in the primary host, we discovered that exposing the skin to UV radiation altered some types of immune responses, including the immune response against skin cancers. Studies on the nature and mechanism of the immunological alterations brought about by exposure to UV radiation suggested that UV-induced DNA damage triggers a cascade of events, leading ultimately to a state of antigen-specific, systemic T lymphocyte-mediated immunosuppression. Key components of this cascade are epidermal cytokines, which modulate the immune response to antigens introduced into the UV-irradiated host and divert the response toward a state of specific immunosuppression. The finding that UV radiation can redirect the immune response from an effector to a suppressor pathway has raised the possibility that immune responses to infectious diseases might also be influenced by exposure of the host to UV radiation. Interest in the health consequences of stratospheric ozone depletion, with its attendant increase in solar UV-B radiation, has stimulated recent investigations on the effects of UV radiation on the pathogenesis of infections in animal models and on immune responses in humans. In addition, attempts are being made to use information about UV-induced specific immunosuppression to eliminate unwanted immune responses, such as transplant rejection and graft-versus-host reactions. Thus, studies on the immunological effects of UV radiation are providing new information on how immune responses are regulated as well as improving our understanding of the role of the immune system in skin cancer induction. This information should facilitate the development of more effective measures for preventing the deleterious effects of overexposure to UV radiation.

Animals↗
PubMed1984

Effects of methoxsalen plus near-ultraviolet radiation or mid-ultraviolet radiation on immunologic mechanisms.

Skin cancers induced in mice by UVB, i.e., 280-320 nm radiation, are highly antigenic. They grow progressively in UVB-irradiated hosts because of certain specific immunologic alterations that are induced in the mice. Comparative studies of the immunologic aspects of carcinogenesis by UVB or methoxsalen plus UVA, i.e., 320-400 nm radiation (PUVA), formed the basis for the following conclusions: 1) Skin cancers induced by PUVA in C3H/HeN mammary tumor virus-negative mice are not highly antigenic, in contrast to those induced by UVB; 2) PUVA-induced tumors also differ from those induced by UVB, in that they do not exhibit preferential growth in UVB-irradiated mice; 3) PUVA treatment of mice, unlike UVB, does not induce susceptibility to the transplantation of UVB-induced tumors; 4) both UVB and PUVA treatments suppress the induction of contact hypersensitivity by a mechanism that involves suppressor lymphocytes.

Animals↗
PubMed1987

[Secondary immunologic deficiency and its correction in cancer patients after radiation and combined therapy].

The problems of radiation immunology in oncological practice are discussed using, by way of example, studies on the effect of radiation and combined therapy on the state of the immunity system in some cancer types. The authors present data on the development of secondary immunodeficiency states determined by disorder in lymphocyte level, cooperation, enzymatic properties and function in immune reactions. A possibility of correction of secondary immunodeficiency states after radiation and combined therapy with the help of immunomodulators was shown.

Adjuvants, Immunologic↗
PubMed1986

Radiation-induced, immunologically mediated regression of an established tumor as an example of successful therapeutic immunomanipulation. Preferential elimination of suppressor T cells allows sustained production of effector T cells.

The results of this study confirm results published by others by showing that sublethal whole-body irradiation of mice bearing immunogenic tumors can result in complete tumor regression. The results show, in addition, that irradiation-induced tumor regression can be prevented by infusion, after irradiation, of Ly-1+,2-,L3T4+ suppressor T cells from the spleens of donors bearing an established tumor, but not by infusion of normal spleen cells. This evidence, plus the demonstration that irradiation fails to cause regression of tumors growing in immunocompetent mice, is consistent with the hypothesis that irradiation-induced regression is immunologically mediated, and that it depends on the ability of irradiation to preferentially eliminate suppressor T cells. By using passive transfer assays to measure the production of effector T cells and suppressor T cells against time of tumor growth, it was shown that irradiation of tumor-bearing mice on day 5 of tumor growth resulted in a failure to generate suppressor T cells on the one hand, and in a sustained production, effector T cells on the other. In other words, irradiation prevented the concomitant antitumor immune response from being downregulated by suppressor T cells. However, giving radiation on day 1 of tumor growth, in contrast to giving it 3-6 d later, caused immunodepression and enhancement of tumor growth. This is in keeping with published evidence showing that, whereas resting effector T cells are highly radiosensitive, antigen-activated effector T cells are relatively radioresistant. It is suggested that the radioresistance of activated effector T cells, coupled with the radiosensitivity of activated suppressor T cells, is the reason for the selectivity of ionizing radiation for suppressor T cells and why a tumor needs to be palpable to undergo regression in response to radiation therapy.

Animals↗