The occurrence of antinuclear basal cell antibodies (ANA) in eluates of lymphoid cells and polymorphonuclear leukocytes obtained in 7 untreated psoriasis patients could be demonstrated by means of the indirect immunofluorescence technique. These antibodies appear to be non-species-specific and are mainly directed against the nuclei of the basal cell layer of uninvolved skin, but also ANA directed against the nuclei of epidermal and dermal cells have been encountered. Moreover a significant decrease of circulating lymphoid cells forming rosettes with sheep erythrocytes has been found in the patients studied, suggesting a diminution of the T-cell control. The immunological mechanisms in psoriasis may therefore be looked upon as being the result of a lack of certain T-cell suppressor genes facilitating the recognition of nuclear basal cell self antigens and a subsequent production of multiclonal antibasal cell nuclear antibodies. These antibodies may interfere with the function of membrane bound enzymes which serve as a regulatory epidermal control mechanism. Various exogenous and endogenous factors may help to initiate the immune response leading to a delayed type reaction at the onset of a lesion and an Arthus type reaction located in the upper layers of the epidermis at a later stage of the disease. Consequently the course of events in psoriasis is a self perpetuating inflammatory process.
|Translated title of the contribution||Immunogenetic aspects of the pathogenesis of psoriasis|
|Number of pages||15|
|Publication status||Published - Dec 1 1977|
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