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Biomedical subjects

C Pincelli

Publications and source records attributed to C Pincelli.

54 records · Page 3Linked to original sources
PubMed1989

Possible role of natural killer cells in granulomatous inflammation.

Natural killer (NK) cell activity is down-regulated in patients with active chronic inflammatory processes, and appears abnormal in sarcoidosis. We investigated NK cell activity in lymph nodes (LN) and spleen cells of C57BL/6 mice by using a 51Cr-release assay against Yac-1 tumor target cells. Hepatic granulomas were caused by infection with 75 cercariae of Schistsoma mansoni ans skin granulomas formed by transplanting isolated liver granulomas into skin of another group of naive mice. Also, anti-NK-1.1 MoAb was injected intraperitoneally into some mice (1 mg IgG/mouse) 1 wk before and weekly for 4 wks after grafting; control mice received saline. Well-organized granulomas appeared in both liver and skin. NK activity (%) was markedly reduce in LN and spleen: (table; see text) The results showed a relationship between granuloma formation and reduction of NK cell activity; both systemically and locally. MoAb did not alter total LN and spleen cell numbers, but reduced NK cell activity by 70-90%. Mean diameter of skin granulomas developed in treated mice was greater (p less than 0.05). NK cells may act as suppressor cells in granulomatous inflammation.

Animals↗
PubMed1988

Skin granuloma formation in mice immunosuppressed by cyclosporine.

Granulomatous tissue reactions appear in athymic mouse skin, indicating that initiation of granuloma formation may be T-cell independent. To further evaluate the relationships between granuloma formation and T-cell function, we treated euthymic BALB/c mice with cyclosporine (Cs), a potent immunosuppressive drug, injected intramuscularly (150 mg/kg/day) 5 times a week. Hepatic granulomas were isolated from mice with schistosomiasis and transplanted into the skin of mice treated with Cs for 2 weeks. Cyclosporine injection was continued for 3 additional weeks. Blood levels of the drug increased during treatment (489 ng/ml at 2 weeks and 822 ng/ml at 5 weeks). Morphologically identical granulomas developed in both treated and untreated mice. Examination for T-cell functions showed that by the end of 2 weeks treatment, concanavalin A, phytohemagglutinin responses, and IL-2 activity were markedly depressed, and IL-2 receptor expression was not detected in either lymph nodes or spleen of the Cs-treated mice; however, after hepatic granuloma graft, T-cell functions in regional lymph nodes, but not in spleen, as well as peripheral blood eosinophilia were stimulated in Cs-treated mice. These data strongly suggest that intact T-cell activity is not essential for the initiation of granuloma formation. In addition, granuloma grafts appear to stimulate Cs-resistant T-cell activation locally, which amplifies and organizes the granulomatous response.

Animals↗
PubMed1988

T-cell depletion by monoclonal antibodies does not prevent granuloma formation in mice.

Effects of T-cell depletion on the formation of organized granulomas in mouse skin were investigated. Monoclonal antibodies (MoAbs) to L3T4 and Lyt-2.2 were injected into euthymic BALB/c mice in order to deplete both T-helper and T-suppressor cell populations. Four days after injection, hepatic schistosome egg granulomas were transplanted into the skin. Injection of MoAbs to L3T4 and Lyt-2.2 was repeated in the recipient mice 6 days later. At the time of transplantation, flow cytometric analysis showed that the number of T cells which were positively stained with surface markers decreased on average by 68% in both regional lymph nodes and spleen. The mitogen response of spleen cells was also markedly reduced. Despite their immunosuppressed condition, development of organized granulomas was observed in the skin of recipient mice by light and electron microscopy 3 weeks after transplantation. The findings indicate that T-cell function may not be essential for initiation of organized granuloma formation.

Animals↗
PubMed1988

Immunopathologic studies in pityriasis lichenoides.

Skin biopsy specimens from five patients with pityriasis lichenoides et varioliformis acuta and from six patients with pityriasis lichenoides chronica were studied by direct immunofluorescence and by an immunoperoxidase technique using a panel of monoclonal antibodies. The dermal inflammatory infiltrate was composed of T cells, macrophages, and a small proportion of CD1a+ cells, mostly perivascular. CD8+ cells (cytotoxic/suppressor phenotype) predominated in the epidermis according to the degree of epidermal necroses, whereas CD4+ cells (helper/inducer phenotype) were superior in number among dermal T cells. A few B cells and Leu7+ cells were detected in only a small proportion of lesions. The results obtained confirm that the two conditions are variants of a single disease process and suggest that cell-mediated immune mechanisms may be important in the pathogenesis of the epidermal and vascular damage. Endothelial cells (HLA-DR+ and HLA-DQ+) and CD1a+ cells (epidermal and possibly dermal) could be primarily involved, acting as antigen-presenting cells.

Adolescent↗
PubMed1986

Effect of selective enzymatic digestions on skin biopsies from pseudoxanthoma elasticum: an ultrastructural study.

Skin biopsies from patients with pseudoxanthoma elasticum (PXE) were studied by electron microscopy either before or after selective digestions with collagenase, elastase, trypsin, hyaluronidase, chondroitinase AC and ABC, with the aim of identifying an eventual organic component associated with mineralization within the elastin fibers and the chemical nature of the enormous aggregates of filaments very often associated with, but distinct from mineralized elastin fibers. The results obtained, on both embedded thin sections and fresh tissue fragments, showed that elastin fibers, whether mineralized or not, were sensitive only to elastase, and they did not contain significant amounts of materials different from elastin that could be accounted for by ion precipitation; the aggregates of microfilaments in strict connection with altered elastin fibers were mostly sensitive to elastase and hyaluronidase, were partially removed by trypsin and chondroitinase, and were not modified by collagenase, which seems to indicate that the microfilaments consist mainly of abnormally aggregated elastin molecules together with low sulfated proteoglycans. It may be concluded that PXE is a complex genetic disorder of the connective tissue, and that mineralization of elastin is only one of the alterations of the extracellular matrix.

Actin Cytoskeleton↗
PubMedDate not supplied

Neuron-specific enolase is a marker of cutaneous Langerhans' cell histiocytosis ("X")-a comparative study with S100 protein.

The immunohistochemical expression of neuron-specific enolase (gamma/gamma) (NSE) was studied comparatively with S100 protein in a group of Langerhans-cell-type ("X") (n = 8) and non-Langerhans-cell-type ("non X") (n = 24) cutaneous histiocytoses. NSE was expressed by the majority (70-90%) of histiocytic cells in all cases of Langerhans-cell histiocytoses, whereas it was absent from non-Langerhans-cell histiocytoses. S100 protein was expressed by the majority of Langerhans-cell histiocytosis cells but also by a small percentage (1-5%) of cells in non Langerhans-cell histiocytoses. These results show that NSE is almost as sensitive as, but more specific than, S100 protein in discriminating Langerhans-cell from non-Langerhans cell cutaneous histiocytoses, and that it consequently represents a useful adjunct in the immunohistochemical diagnosis of histiocytic skin diseases.

Biomarkers↗