Biomedical subjects
Publications and source records attributed to F Facchetti.
Skin biopsies from two children with juvenile xanthogranuloma were studied. Enzyme- and immunohistochemistry was used to establish the mononuclear phagocytic nature of the proliferating dermal elements. The usefulness of both techniques in the diagnosis and the differential diagnosis of this disease is suggested.
We used immunohistochemistry to study Langerhans cells (LCs) and the composition of the dermal inflammatory infiltrate both in normal skin and in biopsies from various benign and malignant pigment-cell lesions. In normal skin and most benign pigment-cell lesions, epidermal LCs are regularly distributed. OKT6-Positive cells outnumber the OKIa-positive cells. The inconspicuous dermal infiltrate studied in these biopsies was composed of helper and suppressor/cytotoxic T cells and some dermal LCs. More epidermal LCs with an abnormal cytologic presentation were found in a halo naevus and in the radial growth part of primary malignant melanomas. This finding was associated with a dermal infiltrate composed of suppressor/cytotoxic T cells, suggesting a defense mechanism of the host towards abnormal melanocytes. Epidermal LCs were rare in the central part of the biopsies which showed a primary malignant melanoma in its vertical growth. A dermal inflammatory infiltrate was absent in that area. These findings are interpreted as the morphologic expression of a damaged immune system.
In four cases of sarcoidal and five cases of tuberculous lymphadenitis, the cellular composition of hypersensitivity-type granulomas was investigated by the application of monoclonal and polyclonal antibodies to cryostat sections. The composition of the granulomas was the same in the two disorders; they consisted of centrally placed OKM1 + OKIa + epithelioid histiocytes and multinucleated giant cells, together with few OKT4 + helper/inducer and many OKT8 + suppressor/cytotoxic T lymphocytes, some of which expressed Ia-like antigens. B lymphocytes were notably absent from this central part but formed a mantle around each granuloma and expressed predominantly or only IgD at their surfaces. Between the perigranulomatous cuff and the central epithelioid histiocytes, OKT8 + lymphocytes were distributed in a ring-like manner. The results suggest that the underlying immunologic mechanisms in sarcoidosis and tuberculosis are similar. Multinucleated giant cells may function as antigen-processing and -presenting accessory cells, and activated T cells, of either the helper or the suppressor type, may be operative in delayed-type hypersensitivity reactions. The presence of a predominance of IgD or of IgD alone at the surface of the perigranulomatous B lymphocytes may be related to a block in their terminal maturation stage, a defect in accessory cells, the presence of a local population of suppressor cells, or to the importance of IgD in granulomatous disorders.
Lymphocyte subsets were analyzed in peripheral blood and lymph nodes from a drug-addict with acquired immunodeficiency syndrome (AIDS) presenting with disseminated lymphadenopathic and oropharyngeal Kaposi's sarcoma. At the onset of disease, hypergammaglobulinemia, increase of OKT8+ T cell subset and reversal of OKT4/OKT8 ratio were found in the blood. At the same time, lymph nodes displayed, besides Kaposi's sarcoma, marked follicular hyperplasia, plasmocytosis and increase of OKT8+/Leu 2a+ T cells within follicular centers. These results are interpreted to indicate that at an early stage of disease the major tissue alterations took place within follicular centers and consisted of both B cell activation and T suppressor cell reaction. These changes correlated with immunological abnormalities observed in peripheral blood. Immunohistochemical investigation of lymphoid tissue may be useful to detect AIDS patients at an early stage.
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Thirty-eight patients with essential mixed cryoglobulinemia (EMC: 16 type II and 22 type III) were evaluated. Almost all patients had clinical manifestations which could be related to a cutaneous and/or visceral vasculitic process. No significant clinical or laboratory differences were found between type II and type III EMC patients. Kidney biopsy performed in 9 patients showed membranoproliferative glomerulonephritis in 6 cases, diffuse proliferative glomerulonephritis in 2 cases and mesangioproliferative glomerulonephritis in one case. Skin biopsy performed in 11 patients showed typical leukocytoclastic vasculitis as the most common finding. A picture consistent with overlapping vasculitis was found in 2 cases (one type II and one type III) and thrombus-like deposits were observed in 3 cases (2 type II and one type III). These thrombotic lesions, not associated with vessel wall necrosis and inflammatory infiltrate, were indistinguishable from those observed in one case of type I cryoglobulinemia. Our data emphasize the complexity of blood vessel involvement in cryoglobulinemia and point out the possible existence of multiple pathogenetic mechanisms.
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Plasmacytoid monocytes, the so-called plasmacytoid T cells, were originally described in rare cases of lymphadenitis. Recent immunohistochemical studies have demonstrated their monocytic origin. Plasmacytoid monocytes have in common with epithelioid cells and multinucleated giant cells the expression of several antigens; they also occur in close topographic association with epithelioid and multinucleated giant cells in epithelioid cell granulomas. On the basis of these data it has been suggested that plasmacytoid monocytes may transform into epithelioid cells. The present ultrastructural and immunoelectron microscopic study of epithelioid cell granulomas provides further arguments in favor of this hypothesis. Moreover, the existence of a transitional cell type with characteristics of plasmacytoid monocytes and epithelioid cells is documented. Subplasmalemmal linear densities present on focal areas of the plasma membrane of the main cell components of granulomas are also discussed.
The skin is one of the most commonly involved tissue in rheumatic autoimmune diseases. Different mechanisms are thought to be implicated in the pathogenesis of skin lesions. In genetically predisposed individuals, ultraviolet (UV) light can contribute to the induction of skin lesions via an inflammatory process. UV light promotes the release of cytokines by keratinocytes and the induction of adhesion molecules on the surface of epidermal cells initiating a cascade of inflammatory events and recruiting immunoinflammatory cells into the skin. In this review data regarding the expression of TNF-alpha in lesional skin tissue from subacute cutaneous lupus erythematosus patients and the role of interferons in the pathogenesis of skin manifestations of rheumatic autoimmune diseases are reported. In addition, an overview on the expression of cellular adhesion molecules in these diseases is provided.UV light can also induce apoptosis in keratinocytes. During this cell death several enzymes became activated. Among them, desoxyribonuclease (DNase) is an enzyme involved in degrading DNA during apoptosis. Data regarding the activity of DNAse in patients with cutaneous lupus erythematosus as a possible risk factor for the development of systemic disease are here reported.
Three patients with Crosti's lymphoma were treated with radiotherapy using electron accelerators. The energy radiations ranged from 5 to 9 Mev. with large fields. The total dose was 40 Gy, delivered in 2 Gy fractions daily. The treatment lasted four weeks. No side effects were reported and no recurrence was remarked after 24 months.
Six cases of disseminated actinic superficial porokeratosis are reported in kidney transplant recipients. Immunohistochemistry study showed an altered state of Langerhans cell surface markers at the level of the cutaneous lesions of porokeratosis. We can hypothesize that the alterate state of epidermal dendritic cells in porokeratosis contributes to the development of abnormal clones of keratinocytes.
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