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Ψ-3 is a monoclonal antibody that recognizes a 135,000 molecular weight structural component of maturing keratinocytes in psoriasis (the Ψ-3 antigen) but fails to bind to any constituent of keratinocytes in normal epidermis. This paper describes the occurrence of the Ψ-3 antigen in a variety of dermatopathologic conditions using immunoperoxidase (biotin-avidin-peroxidase) and immunofluorescence methods which show excellent concordance. In 35 of 36 specimens of psoriasis vulgaris, Ψ-3 antibody consistently immunolabels the cytoplasm of keratinocytes above the basal layer. At the edges of psoriatic plaques, Ψ-3 antibody staining extends for a variable distance into lesion-free epidermis. A similar pattern has been found in a certain number of other conditions described in the paper, including squamous cell carcinoma and condyloma acuminatum, but not Darier's disease basal cell carcinoma, nor lamellar ichthyosis. In all but one condition, the outermost or basal layer of cells is never stained. The only disease in which the lowermost cell layer is stained is a lichen planus-like lesion. The occurrence of Ψ-3 antigen cannot be correlated with any histologic feature of psoriasis such as acanthosis, loss of the granular layer, or hyperproliferation. The antigen appears to be a unique keratinocyte constituent which is expressed in certain pathologic conditions and which is not detected by any other histologic or immunophenotyping method. It is a potentially valuable addition to the panel of antibodies available for characterizing epithelial cells. [ABSTRACT FROM AUTHOR]

This article presents abstracts for various research papers to be presented in the European Society for Dermatological Research's symposium on September 26-28, 1997. These research papers pertain to subjects like the eortic classification for primary cutaneous lymphomas, different prognosis between cutaneous and systemic lymphoproliferative disorders, parapsoriasis and early cutaneous T cell lymphoma, immunoglobulin gene rearrangement of pseudo B-cell lymphomas and prognostic significance of polymerase chain reaction detectable dominant T lymphocyte clones.

This paper details current and historic epidemiologic features of Fogo Selvagem (Endemic pemphigus foliaceus) in Brazil. The following features arc described, a) The disease occurs in endemic fashion in regions of Brazil within the states of Goias, Mato Grosso do Sul, Parana, Sao Paulo, and Minas Gerais. It appears that the disease is spreading toward the northwest and west, involving the states of Mato Grosso, Para, Maranhao, Rondonia, Acre, and Arnazonas. b) People at risk are young peasants or children of either sex or any race exposed to the local ecology in rural areas of endemic states. Although the disease has been described in urban centers, these occurrences are rare. c) Fogo Selvagem commonly appears in wild areas being colonized and disappears as these areas become urbanized. d) The majority of patients live in close proximity to rivers and within the 10-15 Km flying range of mosquitos or black flies (such as Simulium). It is hypothesized that a black fly, Simulium pruinosum may be the vector that precipitates the disease. f) There is a significant number of Fogo Selvagem in family units where multiple, genetically related individuals are affected. g) Finally, autoantibodies against lupus-associated antigens are not present in the sera of patients with Fogo Selvagem. Clinical examination of the skin, and serologic screening for pemphigus autoantibodies are specific parameters that can be used in the search for the etiologic agents that lead to autoimmune disease of the skin. To identify and prove an etiologic agent for this well-characterized autoimmune disease would be of tremendous importance to the understanding of autoimmune skin diseases, and potentially other organ-specific autoimmune disorders. [ABSTRACT FROM AUTHOR]

Photosensitivity associated with lupus erythematosus (LE) is well established. The photobiologic basis for this abnormal response to ultraviolet radiation, however, has not been determined. This paper summarizes the criteria for elucidating possible photobiologic mechanisms and reviews the literature relevant to the mechanism of photosensitivity in LE. In patients with LE, photosensitivity to wavelengths shorter than 320 nm has been demonstrated; wavelengths longer than 320 nm have not been adequately evaluated. DNA is a possible chromophore for photosensitivity below 320 nm. UV irradiation of skin produces thymine photodimers in DNA. UV-irradiated DNA is more antigenic than native DNA and the antigenicity of UV-irradiated DNA has been proposed, but not proven, to be involved in the development of clinical lesions. UV irradiation of mice previously injected with anti-UV-DNA antibodies produces Ig deposition and complement fixation that appears to be similar to the changes seen in lupus lesions. Antibodies to UV-irradiated DNA occur in the serum of LE patients although a correlation between antibody titers and photosensitivity was not observed. Defective repair of UV-induced DNA damage does not appear to be a mechanism for the photosensitivity in LE. Other mechanisms must also be considered. The chromophore for photosensitivity induced by wavelengths longer than 320 nm has not been investigated in vivo. In vitro studies indicate that 360-400 nm radiation activates a photosensitizing compound in the lymphocytes and serum of LE patients and causes chromosomal aberrations and cell death. The mechanism appears to involve superoxide anion. Further research is required to establish the action spectrum for long wavelength photosensitivity in vivo and to elucidate the mechanisms for the photosensitivity at all wavelengths. [ABSTRACT FROM AUTHOR]

In this paper we report the use of immunological methods for specifically detecting and determining proteoglycan in cartilage and other connective tissues. Antibodies (polyclonal and monoclonal) have been raised against specific components of cartilage proteoglycan aggregates (i.e., proteoglycan monomer and link protein). Radioimmunoassay procedures and immunohistochemical procedures have been developed and used to demonstrate the occurrence of cartilage-like proteoglycan and link protein in bovine aorta. Similarly, immunofluorescent studies have been used to analyze proteoglycan distribution in skin. Using antibodies specific for chondroitin-4-sulfated proteoglycan, their presence was demonstrated in dermal connective tissue and connective tissue surrounding nerve and muscle sheaths. However, chondroitin-4-sulfated proteoglycan was completely absent in the epidermis of skin and areas surrounding invaginating hair follicles. These immunological procedures are currently being used to complement conventional biochemical analyses of proteoglycans found in different connective tissue matrices. [ABSTRACT FROM AUTHOR]

It has been suggested that the bulge of the hair follicle contains a poll of follicular stem cells that may serve as a target site of graft-versus-host disease and as a source of cells with carcinogenic potential. The bulge is prominent in the developing follicle although it is a subtle swelling in the adult follicle. In this paper, we studied the bulge in human fetal skin specimens. Ultrastructurally, the bulge cells, especially the interior cells, have abundant free ribosomes and glycogen particles, but almost no cytoplasmic organelles indicative of differentiation. Immunostaining with several specific anti-keratin antibodies demonstrated that the bulge cells express keratins of both stratified and simple epithelia. Melanocytes and Merkel cells, defined by immunohistochemical and ultrastructural criteria, are seen among bulge cells. Laser confocal microscopy revealed that primitive smooth muscle cells attached directly to the bulge initially at the mid-bulbous hair peg, the stage when the bulge is most prominent. K-laminin and type VII collagen are strongly expressed in the dermoepidermal junction of the bulge and between the matrix area of the bulb and the dermal papilla. Thus, the bulge of human hair follicle is not only an attachment site for arrector pili muscle, but also a pool of keratinocytes that are relatively undifferentiated. [ABSTRACT FROM AUTHOR]

Recent papers have reported that there are at least two distinct binding sites of bullous pemphigoid (BP) antibodies; one is the extracellular (lamina lucida) BP antigen (E-BPA) and the other is the intracellular (basal cell cytomembrane-hemidesmosome-cytoskeleton) BP antigen (I-BPA). In attempting to characterize the properties of these two BP antigens (BPA), we have investigated the expression of E-BPA and I-BPA as well as other basement membrane zone (BMZ) components such as type IV collagen, laminin, and epidermolysis bullosa acquisita (EBA) antigen at the dermal-epibolic junction as a model system for BMZ neogenesis. I-BPA was found along the dermal-epidermal junction and throughout the whole length of the dermal-epibolic junction. However, E-BPA and other BMZ components were found along the dermal-epidermal junction and along only the most proximal portion of the dermal-epibolic junction. These results suggest 1) that emergence of E-BPA varies from that of I-BPA in such a model system of BMZ neogenesis, and 2) that the emerged E-BPA may attach to the newly formed basement membrane complex. [ABSTRACT FROM AUTHOR]

The article presents an overview of papers on skin diseases that appears in the March 1996 issue of the journal "The Journal of Investigative Dermatology." One of the paper describes a patient with a novel blistering disease with antibodies to a 200 kD lamina lucida autoantigen. In another paper, scientists provide additional proof of adherens junctions in skin. In another paper, scientists demonstrate the occurrence of two closely spaced polymorphic sites in the helix termination region of the cuticular hair keratin gene that lead to the substitution either of a highly conserved threonine by methionine or of a conserved serine by asparagine.

The present paper describes a new in vivo method to study the action of pemphigus antibodies against human tissue. Oral mucosal biopsies from healthy donors were transplanted to athymic nude mice, which, a week later, were injected with serum from pemphigus patients. From 1 to 5 days after the injection the epithelial transplants were removed and preparations were studied by immunofluorescence microscopy. Pemphigus antibodies were demonstrated in preparations from each of 23 mice which had received pemphigus serum, but in none of 6 which had received control serum. Transplants from about ⅔ of the experimental mice showed intercellular edema of the basal layers of the epithelium and in transplants from 3 mice supra-basilar splitting of the epithelium was found. None of these changes was seen in the control mice. Passive transfer of human serum or lymphocytes to nude mice transplanted with human tissue may be of use in future studies of autoimmune diseases, including pemphigus. [ABSTRACT FROM AUTHOR]