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PubMedDate not supplied

[Immunomodulating and antioxidant effects of magnetic and laser irradiation combined with administration of beta-carotene, essentiale, and riboxine during cold stress].

We studied effects of beta-carotine, essentiale and riboxine on immunometabolic effects induced by laser or magnetic laser radiation in intact rats and rats exposed to immersion cold. We found that combination of laser or magnetic laser radiation with administration of beta-carotine or riboxine more effectively corrected antioxidant status and immunological reactivity than radiation alone or in combination with essentiale.

Adjuvants, Immunologic↗
PubMed1991

Effect of chronic microwave radiation on T cell-mediated immunity in the rabbit.

Experiments were conducted to elucidate the effects of chronic low power-level microwave radiation on the immunological systems of rabbits. Fourteen male Belgian white rabbits were exposed to microwave radiation at 5 mW/cm2, 2.1 GHz, 3 h daily, 6 days/week for 3 months in two batches of 7 each in specially designed miniature anechoic chambers. Seven rabbits were subjected to sham exposure for identical duration. The microwave energy was provided through S band standard gain horns connected to a 4K3SJ2 Klystron power amplifier. The first batch of animals were assessed for T lymphocyte-mediated cellular immune response mechanisms and the second batch of animals for B lymphocyte-mediated humoral immune response mechanisms. The peripheral blood samples collected monthly during microwave/sham exposure and during follow-up (5/14 days after termination of exposures, in the second batch animals only) were analysed for T lymphocyte numbers and their mitogen responsiveness to ConA and PHA. Significant suppression of T lymphocyte numbers was noted in the microwave group at 2 months (P less than 0.01, delta % 21.5%) and during follow-up (P less than 0.01, delta % 30.2%). The first batch animals were initially sensitised with BCG and challenged with tuberculin (0.03 ml) at the termination of microwave irradiation/sham exposure and the increase in foot pad thickness (delta mm), which is a measure of T cell-mediated immunity (delayed type hypersensitivity response, DTH) was noted in both the groups. The microwave group revealed a better response than the control group (delta % +12.4 vs. +7.54). The animals were sacrificed and the tissue T lymphocyte counts (spleen and lymph node) were analysed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Ultraviolet A radiation (320-400 nm) protects hairless mice from immunosuppression induced by ultraviolet B radiation (280-320 nm) or cis-urocanic acid.

T cell-mediated immune function, here measured as the contact hypersensitivity reaction, is readily suppressed by moderate exposure of mice to ultraviolet B (UVB) or solar-simulated radiation (SSUV), or by topical application of cis-urocanic acid. The effect of ultraviolet A (UVA) radiation on immune function has been unclear. Here we have demonstrated that when UVA radiation from a fluorescent tube source was rigorously filtered to remove contaminating UVB radiation, it was immunologically innocuous at physiologically relevant doses. Furthermore, we have found that mice exposed to UVA radiation, either immediately after, or up to 24 h before, immunosuppressive treatment with either UVB radiation, SSUV or cis-urocanic acid, became refractory to the immunosuppression and retained more normal contact hypersensitivity. A greater UVA exposure reversed the immunosuppression more effectively. The results suggest that there are immunologically significant interactions between UV wavebands, and that UVA exposure may induce a relatively long-lived immunoprotective photoproduct, as yet unidentified, that can inhibit the activity of epidermal cis-urocanic acid and thus provide protection from photoimmunosuppression.

Animals↗
PubMed2003

Global surface ultraviolet radiation intensity may modulate the clinical and immunologic expression of autoimmune muscle disease.

OBJECTIVE: To determine if geoclimatic factors may influence the nature and frequency of dermatomyositis (DM), polymyositis, and associated autoantibodies around the world. METHODS: We assessed, in the first global evaluation of these conditions, the relationship between 13 geoclimatic variables that may modulate disease and the relative proportion of DM and its associated autoantibody anti-Mi-2, directed against an SNF2-superfamily helicase associated with the nucleosome remodeling and histone acetylation and deacetylation complex, in a global myositis population. Altogether, 919 consecutive patients from populations at 15 locations were studied. RESULTS: Univariate and multivariate analyses demonstrated that of the variables evaluated, surface ultraviolet (UV) radiation intensity (irradiance) most strongly contributed to the relative proportion of DM and was strongly related to the proportion of anti-Mi-2 autoantibodies (weighted r = 0.939, P < 4 x 10(-7) and weighted r = 0.69, P = 0.02, respectively). Published ethnogeographic immunogenetic allele frequencies imply that the striking differences in the proportion of DM- and DM-specific autoantibodies observed around the world are not the result of inherent global variations in known genetic risk factors. CONCLUSION: These data suggest that UV radiation exposure may modulate the clinical and immunologic expression of an autoimmune disease in different populations around the world.

Autoantibodies↗
PubMed2001

Identification of KIN (KIN17), a human gene encoding a nuclear DNA-binding protein, as a novel component of the TP53-independent response to ionizing radiation.

Ionizing radiation elicits a genetic response in human cells that allows cell survival. The human KIN (also known as KIN17) gene encodes a 45-kDa nuclear DNA-binding protein that participates in the response to UVC radiation and is immunologically related to the bacterial RecA protein. We report for the first time that ionizing radiation and bleomycin, a radiomimetic drug, which produce single- and double-strand breaks, increased expression of KIN in human cells established from tumors, including MeWo melanoma, MCF7 breast adenocarcinoma, and ATM+ GM3657 lymphoblast cells. KIN expression increased rapidly in a dose-dependent manner after irradiation. Under the same conditions, several genes controlled by TP53 were induced with kinetics similar to that of KIN. Using the CDKN1A gene as a marker of TP53 responsiveness, we analyzed the up-regulation of KIN and showed that is independent of the status of TP53 and ATM. In contrast, the presence of a dominant mutant for activating transcription factor 2 (ATF2) completely abolished the up-regulation of KIN. Our results suggest a role for ATF2 in the TP53-independent increase in KIN expression after gamma irradiation.

Activating Transcription Factor 2↗
PubMed1984

The effect of a sunscreen containing para-aminobenzoic acid on the systemic immunologic alterations induced in mice by exposure to UVB radiation.

Application of a sunscreen containing para-aminobenzoic acid partially abrogated certain of the systemic immunologic alterations produced in mice by exposure to UVB (280-320 nm) radiation from sunlamp bulbs. The sunscreen reduced the degree of UVB-induced suppression of contact hypersensitivity to a chemical applied subsequently to nonirradiated skin. In addition, it reduced the frequency with which mice became susceptible to the growth of a highly antigenic, syngeneic, UVB-induced tumor following chronic treatment with UVB radiation, but this effect was not statistically significant. The tumor-susceptible state was transferred from animals treated with sunscreen and UVB radiation to lethally x-irradiated mice by injection of spleen cells. The gross morphology of the skin of mice treated with sunscreen and UVB radiation was normal but the histologic changes induced by UVB irradiation in skin were only partially abrogated by the sunscreen.

4-Aminobenzoic Acid↗
PubMed1978

Immunologic aspects of tumor induction by ultraviolet radiation.

Chronic treatment of mice with UVR not only induced skin cancer but also produced a systemic change that interfered with host resistance against these tumors. The studies leading to the this conclusion were prompted by the discovery that most tumors induced in C3H mice by chronic UV irradiation were immunologically rejected following transplatation to normal syngeneic recipients. This raised the question of why these tumors were able to grow progressively in the autochthonous host without being destroyed immunologically. We found that after a short course of UV treatment, the UV-irradiated mice lost their ability to reject transplanted UV-irradiated mice lost their ability to reject transplanted UV-induced tumors, even though such transplants were rejected by unirradiated animals. The growth of the transplanted tumors in UV-treated mice resulted from a systemic alteration in the animals that was induced by UV irradiation of the skin.

Animals↗