The final destiny of acantholytic cells in pemphigus is Fas mediated.

Background: Pemphigus is an autoimmune disease characterized by the formation of intra-epidermal blisters. Patients develop auto-antibodies against desmoglein 1 and 3 proteins and induce acantholysis.

Objective: This work addresses the issue of whether the Fas pathway mediates acantholysis.

Intracellular antigens released from Balb/c mice kidneys under chemically induced apoptosis and/or necrosis.

The present investigation assesses the possible role of apoptosis and necrosis in intracellular antigen exposure of kidneys from Balb/c mice. Renal tissues were cultured and treated with chemicals to induce apoptosis and /or necrosis. The expression of intracellular antigens Sm, RNP, Ro and La were monitored with antibodies against these antigens.

Production of anti-epithelial antibodies and acantholysis by vaccination with an anti-idiotypic antibody, mimicking desmoglein 1.

Theoretically, the immunization of experimental animals with an anti-idiotype antibody may elicit antibodies that recognize epitopes like the original idiotype; this is archived via internal images. Using this strategy, we attempted to produce anti-epithelial antibodies in Balb/c mice immunized with a pemphigus anti-idiotypic determinant. First, when an anti-idiotype antibody was produced in rabbits by immunization with pemphigus immunoglobulin G (IgG), the anti-idiotypic activity was tested successfully.

The role of apoptosis in autoantibody production.

Apoptosis is the physiologic process that guarantees the cellular exchange; after apoptosis the cellular remains are cleared by phagocytosis. In autoimmunity, some mechanisms in apoptosis fail and may result in disease. For instance, a failure in the Fas pathway during lymphoid ontogeny may allow the survival of autoimmune clones; equally the lack of clearance of apoptotic corps containing self-antigens may activate pre-existent auto-reactive clones and may result in autoantibody production.

Camptothecin induces the transit of FasL trimers to the cell surface in apoptotic HEp-2 cells.

Fas ligand (L) is a membrane protein from the tumor necrosis factor (TNF) family. It induces apoptosis upon contact with its Fas/CD95/APO1 receptor. Trimerization of FasL on the surface of effector cells is essential in the binding of the Fas trimer of the target cells.

Scleroderma with type III glomerulonephritis and MPO-ANCA antibodies in the serum.

Scleroderma is an autoimmune disease characterized by early inflammatory infiltrates followed by fibrosis in the skin and internal organs. CREST is a relatively benign cutaneous variant of scleroderma that features calcinosis, Raynaud's phenomenon, oesophageal dysfunction, sclerodactyly and telangiectases. Glomerulonephritis is a rare association of CREST.

TNFalpha and IL-6 are mediators in the blistering process of pemphigus.

Background: Pemphigus is an autoimmune disease characterized by intraepidermal blisters induced by pemphigus IgG. In addition to autoantibodies, molecular mechanisms involved in acantholysis remain largely unknown. For this reason, we address a possible role of the inflammatory cytokines IL-6 and TNFalpha in pemphigus lesions.

Cellular localization of the Ro/SS-A antigen.

The cellular localization of the Ro/SS-A antigen was defined using indirect immunofluorescence and eight monospecific anti- Ro/SS-A antisera which were identified by immunoblotting. Several mammalian tissues were used as substrates. The Ro/SS-A antigen was located mainly in the nucleus of dog liver and Hep-2-cells, and anti-Ro sera had produced a speckled staining pattern.