Biomedical subjects
Publications and source records attributed to K Holubar.
Linear deposits of both IgA and C3 were found along the BMZ (by direct IF), and band-like IgA deposits directly below the basal lamina (by HRP-anti-HRP electron microscopy), in a case of clinically typical DH. No circulating antibodies could be detected.
IgG and C3 deposits were observed in the basement membrane zone in a case with herpes gestationis. In addition, circulating IgG anti-basement membrane antibodies were found. Electron microscopic immunocytochemical investigations, performed with a peroxidase-antiperoxidase sandwich technique, revealed the in vivo-bound IgG to be localized at the epidermal basal lamina and to exhibit a distribution pattern which is identical to that reported for bullous pemphigoid.
A multistep immunocytochemical method utilizing horseradish peroxidase as an immunologically bound marker was used to detect and localize IgA deposits in skin of patients with dermatitis herpetiformis at the ultrastructural level. IgA was found in the upper papillary dermis forming irregular aggregates in seemingly haphazard distribution. These aggregates were associated with microfibrillar bundles and with the microfibrillar component of the elastic tissue. IgA was also detected on anchoring fibrils, but showed no topical relationship to the basal lamina which was always spared. This finding indicates that basal lamina components do not serve as target sites for the immunologic reaction occurring in dermatitis herpetiformis. The selective affinity of IgA deposits to microbfibrillar bundles may be relevant to the hypothesis that the skin pathology in dermatitis herpetiformis is caused by circulating gluten-antigluten complexes, trapped in the skin by reticulin-bound antireticulin antibodies which cross-react with gluten.
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A multi-step immunocytochemical method utilizing horseradish peroxidase (HRP) as an immunological marker was employed to demonstrate, at the ultrastructural level, IgG antiepithelial autoantibodies bound in vivo to pemphigus epidermis, and circulating IgG antibodies, using monkey oesophagus as substrate. To demonstrate IgG the following antisera were employed in sequential steps: Goat antihuman IgG; rabbit antigoat IgG; goat-anti-HRP-serum. After incubating with the final antigen, HRP, the latter was visualized with a cytochemical method. Results paralleled those obtained by immunofluorescence, the antiepithelial antibody being demonstrated at the sites of the intercellular spaces of the epidermis. Electron microscopic cytochemistry showed IgG in the surface coat of epidermal cells and in the intercellular space, both in the desmosomal and the interdesmosomal areas. These results confirm the results of a previous study but the localization of the antibody is more exact than that obtained with HRP-conjugates. The present method is more versatile and specific than HRP methods that utilize HRP-conjugated antibodies.
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A 43-year-old white man presented with a generalized eruption of lichen planus and tense blisters within the lichenoid lesions and also on clinically normal skin. Direct immunofluorescence (IF) studies revealed immunological and histopathological characteristics of lichen planus in the lichenoid lesions and of bullous pemphigoid in the bullous lesions, and indirect IF studies showed that the patient had circulating antibasement membrane antibodies. The coexistence of both disorders may indicate a possible link between the pathology in the junctional zone in lichen planus and the appearance of antibasement membrane zone antibodies and bullous lesions, respectively.
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