Ultraviolet radiation is absorbed in the skin, especially in the epidermis. After ultraviolet irradiation the number of major histocompatibility complex class II+, adenosine triphosphatase+ Langerhans cells and Thy-1+ dendritic epidermal cells in the epidermis decreases. Whether this decrease is due to migration of these cells or to loss of membrane markers is not clear. To address this question we have used the monoclonal antibody H3 directed against cyclobutyl thymine dimers-a form of DNA damage that is specifically induced by ultraviolet radiation-to investigate whether H3+ cells are present in the draining lymph nodes of the skin after ultraviolet irradiation of hairless, inbred mice (HRA/Skh). After a single dose of ultraviolet radiation (Westinghouse FS40, 1.5 kJ/m2), H3+ cells were present in the paracortex of the draining lymph nodes. No positive cells were found in the blood of irradiated mice. These results suggest that the H3+ cells in the lymph nodes originate from the skin. The number of H3+ cells in the draining lymph nodes increased the first 24 h after irradiation and then stabilized. Immunohistochemical double staining revealed that all H3+ cells were major histocompatibility complex II+, and that only a fraction of the cells were NLDC-145 positive. No V gamma 3 T-cell receptor bearing cells could be found in the lymph nodes after UV irradiation of the skin.
Fruit allergy causes less severe symptoms than TN and especially PN allergy. However, this is not reflected in the prescription or use of emergency medication. This may indicate that physicians are not fully acquainted with the guidelines for prescription of emergency medication. A high impact on daily life was found both in PN, TN and in fruit allergy.
Most of the expenses associated with the 'Coping with itch' programme were incurred during the first 3 months, but the benefits in terms of days with little itch appeared to persist and increase beyond 3 months, thus leading to a more favourable incremental cost-effectiveness ratio.
Experimental evidence is provided to show that ‘classical’ C3 in the serum of patients with pigeon-fancier’s lung – in its acute, subacute or chronic form – is rapidly depleted by incubation with antigens from pigeon excreta. The most effective antigens, which are active in the nanogram range, reside among the aspecifically-precipitating ‘A’ heteropolysaccharides. With the aid of an R3 reagent, a simple laboratory test has been developed which is highly significant for pigeon-breeder’s disease (PBL). The results indicate that C3 inactivation in the serum of these patients is mediated by the – unusually labile – bypass mechanism of complement consumption, without participation of the early components. A discussion is given of the possible contributions of the various antigens in pigeon excreta to the mechanisms of pathogenesis of PBL.
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