[Immunological disorders caused by radiations in the light of a modern theory of immunity].
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As many as 138 patients with acute radiation sickness, grades O-IV, were examined over time. It has been revealed that disorders in microecology and humoral immunity agreed well with the severity of radiation damage.
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A study was made of the effect of combined treatment (routine drug therapy, massage, application of DMSO) alone and in combination with acupuncture and laser puncture on a degree of secondary (radiation) edema and immunological indices in 36 patients treated for breast cancer 2-15 years ago. These methods were shown to decrease effectively a degree of edema by 22-37%. The highest effect was achieved using laser puncture against a background of the main treatment. All types of combined modality treatment promoted the return of the patients' immunological status to normal (an increase in low and a decrease in high values). The most effective recovery was noted in the lymphocyte count, the ratio of helpers (inductors and suppressors) killers, and lymphocyte blast transformation reaction to mitogens.
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Iatrogenic lung disease in man is generated by very different and often complex pathology. This explains the great clinical diversity of these disorders which may manifest as eosinophilic pneumonia, intra-alveolar haemorrhage, bronchiolitis obliterans and diffuse interstitial pneumonia even with pulmonary fibrosis. The causes are also very varied such as direct cellular toxicity, cellular oedema, an alteration of the alveolar capillary membrane, the activation of inflammatory and/or immune cells, which are responsible for the production of soluble mediators whose effects are sometimes harmful to the pulmonary parenchyma. Rather than reporting on the different clinical types of iatrogenic lung disease and indicating for each one the hypothetical or known physiopathogenic mechanism, we have chosen to examine certain fundamental lesional mechanisms and to indicate the principal nosological groups which they cover. We have centered this review on the physiopathogenic models which are the most coherent and most fully elaborated based on observations made on man or on experimental animal models. Among those we have reported here is a case of bleomycin toxicity, with its direct toxic mechanism on the epithelial or endothelial cellular targets, amiodarone lung disease and with its associated alveolar oedema, inflammatory reactions and immunological reactions whose specificity is poorly understood; also there are some alveolitides whose specificity has been demonstrated, such as those to minocycline and to BCG and finally a complex model which is both inflammatory and disturbed immunology in radiation pneumonia.
Transient 19S antibody formation was induced in rabbits by single or repeated stimuli with a small dose of poliovirus. Available evidence indicated that cessation of 19S synthesis was due to lack of continuous antigenic stimulation and not to loss of cells participating in antibody formation. "Immunological memory" in 19S antibody formation was demonstrable only within 2 to 3 days following discontinuation of synthesis but not thereafter. Following stimulation with a high dose of polio-virus both 19S and 7S antibodies were formed. The kinetics of their formation differed in several respects: (a) 19S antibody preceded 7S antibody by 1(1/2) days; (b) 19S antibody rose to peak titers at a rapid exponential rate within 1 week, while 7S antibody increased at a slow decelerating rate for 3 weeks; (c) 19S antibody formation was short-lasting while 7S antibody synthesis endured. A renewed formation of both antibodies occurred following restimulation with a high antigen dose. The secondary 19S and 7S antibody responses were similar to the respective primary responses, and the preexistence of 7S antibody synthesis did not detectably alter the secondary 19S response. Both 19S and 7S antibodies were formed and the kinetics of their formation was similar (a) for infectious and non-infectious (UV-) poliovirus antigen; (b) for the serologically unrelated poliovirus and Coxsackie B-4 virus; (c) when poliovirus was administered by different routes; (d) when 1-day-old or adult rabbits were immunized; (e) in antibody responses to poliovirus in rabbit, guinea pig, and man. Whole body x-irradiation 20 hours prior to antigenic stimulus (high dose) resulted in delayed but markedly prolonged 19S antibody formation and inhibition of 7S antibody synthesis. Thus, the formation of 19S and 7S antibody differed in (a) antigen dose requirements for induction and maintained synthesis; (b) kinetics; (c) retention of memory; and (d) sensitivity to prior x-irradiation. These differences are best explained on the assumption that the two antibodies are produced by different cells.
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The mechanisms that cause skin wrinkling in response to chronic exposure to sunlight are unknown. We investigated the possibility that wrinkling of Skh-1 hairless mice is associated with an ultraviolet (UV) radiation-induced immunologic alteration. Exposing Skh-1 hairless mice to a regimen of nonerythemal UV-B (290-320 nm) radiation induced skin wrinkles after 6-7 weeks. Concomitant treatment with cyclosporin A decreased the time to the onset of wrinkles to approximately 4 weeks. Exposing HRS/J hairless mice or athymic nude mice to a similar nonerythemal UV-B radiation regimen for 10 weeks failed to induce skin wrinkles. Concomitant administration of cyclosporin A and UV-B radiation for 7 weeks to HRS/J hairless mice induced no skin wrinkles. Ultraviolet-B or UV-B plus cyclosporin A exposure caused increased immunohistochemical staining for Ia and F4/80 antigens in the upper dermis of tissue from Skh-1 mice, as compared to controls. Treating Skh-1 mice with UV-B radiation plus cyclosporin A was also associated with a large increase in the number of CD3+ cells in the dermis. These staining patterns were absent in similarly treated HRS/J hairless mice. Dermal mast cell numbers in Skh-1 mice were 2-3-fold higher than in HRS/J, athymic nude or NSA mice. Treatment with cyclosporin A increased Skh-1 dermal mast cell numbers approximately 2-fold but had no effect on the dermal mast cell numbers in HRS/J or NSA mice. Based on these findings we postulate that UV-B light and cyclosporin A exacerbate an immunological condition in Skh-1 mice, one consequence of which is manifested as skin wrinkles. Thus, the induction of skin wrinkles in this mouse strain may have no relevance to the wrinkles observed in human skin after chronic exposure to sunlight.
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