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Y Shoenfeld

Publications and source records attributed to Y Shoenfeld.

At least 613 records · Page 34Linked to original sources
PubMed1991

Idiotype specific T-cell lines inducing experimental systemic lupus erythematosus in mice.

Immunization of mice with either antibodies bearing the 16/6 idiotype (16/6 Id) or anti-idiotypic antibodies against the 16/6 Id induces experimental systemic lupus erythematosus (SLE). We report here the establishment and characterization of 16/6 Id-specific T-cell lines from C3H.SW (H-2b) and BALB/c (H-2d) mice. Both lines proliferate specifically in response to the 16/6 Id in an H-2-restricted manner. The injection of 16/6 Id-specific T cells into syngeneic mice led to the development of experimental SLE. Furthermore, inoculation of the 16/6 Id-specific T-cell line derived from C3H.SW mice into the H-2 compatible C57BL/6 mice, which are non-responders to the 16/6 Id, induced experimental SLE. This report provides direct evidence for the role of idiotype-specific T cells in the induction of experimental SLE.

Animals↗
PubMed1991

The frequency of a common anti-DNA antibody idiotype (16/6) in different populations of patients with systemic lupus erythematosus.

The 16/6 anti-DNA idiotype (id) is a pathogenic idiotype first identified on a human hybridoma antibody derived from a patient with systemic lupus erythematosus (SLE). The SA-1 anti-DNA, which antibody was established in a similar fashion from a patient with polymyositis, also carries the 16/6 id, although it has a greater reactivity with dsDNA. The presence of the 16/6 id as defined by anti-16/6 and anti-SA-1 was determined in 3 distinct populations of patients with SLE: 502 Mexicans, 98 English (including Caucasians, West Indians, Chinese, Asians) and 93 Israelis. A similar prevalence (around 20%) of the 2 idiotypes was found, with a significant overlap. The latter finding was supported by a significant correlation noted between the prevalence of the 2 idiotypes (r = 0.58 p less than 0.001). Despite the fact that 16/6 antibody is most probably encoded by a germline gene, thus being genetically determined, no distinction in the prevalence of the ids could be detected between completely different populations of patients with SLE. This finding may support the independent pathogenic role ascribed to the 16/6 id.

Antibodies, Antinuclear↗
PubMed1991

Chronic infections and autoimmunity.

The studies summarized in this chapter indicate that chronic bacterial, viral, and parasitic infections can serve as a trigger factor of autoimmune reactivity according to various mechanisms. The relationship between microbes and autoimmunity could be manifested by the presence of autoantibodies, autoimmune complexes, or T cells with autoactivity. The presence of autoimmune phenomena in chronic infections could be related to polyclonal B-cell activation, molecular mimicry between microbial and host antigens, altered self, abnormal expression of immunoregulatory molecules, and the anti-idiotypic network. In most cases, the appearance of self-reactivity in the sera of patients with chronic infections is not associated with clinical manifestations. These findings suggest that autoimmune disease is the result of a combination of factors including immunologic, genetic, hormonal, and environmental. Infectious agents have a role in the breakdown of tolerance and the appearance of autoreactivity. However, only patients with the proper immunogenetic and hormonal background may develop clinical manifestations of autoimmune disease. In spite of the extensive knowledge that has accumulated, the specific relationship between infections and autoimmunity is still obscure. Clearly, additional studies are required to clarify the relevance of microbes to the pathogenesis of autoimmune diseases.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Superior vena cava occlusion in a patient with antiphospholipid antibody syndrome.

A 55-year-old woman with a lupus like disease, associated with the lupus anticoagulant, was admitted because of facial edema. Her facial swelling was previously attributed to the steroids she had been taking and they were tapered without improvement. Laboratory tests revealed high titers of anticardiolipin antibodies. Computerized tomography of her chest and Doppler ultrasound examination of her neck veins demonstrated a thrombus in the superior vena cava. She was treated with heparin and was maintained with longterm warfarin therapy with uneventful followup. Superior vena cava obstruction should be added to the long list of thromboembolic complications of the antiphospholipid syndrome.

Antibodies↗
PubMed1991

Determination of autoantibodies in patients with familial Mediterranean fever and their first degree relatives.

Sera samples of 168 patients with familial Mediterranean fever (FMF) and their 184 first degree relatives were analyzed for the presence of autoantibodies to ssDNA, dsDNA, poly (I), poly (G), cardiolipin, histones, RNP and Ro(SSA), using an enzyme linked immunosorbent assay (ELISA). A similar analysis was employed on culture fluids of Epstein-Barr virus (EBV) transformed B lymphocytes derived from patients with FMF and healthy controls. No increased incidence of these antibodies was observed among patients with FMF and their relatives compared to healthy controls. It is possible that autoimmune features observed in FMF are the result of nonspecific changes occurring in inflammation and not due to autoimmune mechanisms.

Antibodies, Antinuclear↗
PubMed1990

Autoantibodies in neoplasia. An unresolved enigma.

One hundred sixty-four sera samples of patients with malignant diseases were analyzed for the presence of autoantibodies to ssDNA, dsDNA, poly(I), Poly(G), cardiolipin, histones, RNP, Sm, Ro(SSA), and La (SSB). No distinction could be made between these patients and a comparative group composed of age-adjusted healthy subjects when measuring antibody levels to these autoantigens by the ELISA technique. This finding remained valid after further subgrouping of the patients according to age, sex, and histologic origin of the tumor. The authors conclude that in contrast to the known clinical coexistence of neoplasia in autoimmune states, there is no increased incidence of antinuclear autoantibodies in malignant conditions.

Adolescent↗
PubMed1990

[Renal crisis in scleroderma with normal blood pressure].

A 58-year-old man with scleroderma affecting many organs, including skin, lung and heart, developed fatal renal failure although his blood pressure was normal. He had been operated on 2 months before when free air was found under the diaphragm following spontaneous rupture of cysts of pneumatosis cystoides intestinalis.

Acute Kidney Injury↗
PubMed1990

Anti-Sm-RNP activity in sera of patients with rheumatic and autoimmune diseases.

The sera of various rheumatic and autoimmune diseases were examined for the presence of anti-RNP/Sm activity. An enzyme-linked immunosorbent assay (ELISA) was employed. Anti-RNP Ab's were detected in 18%, 20%, 28%, 16% of the sera of SLE, myasthenia gravis (MG), rheumatoid arthritis (RA) and thyroid diseases respectively. The anti-RNP Ab's belonged to the IgG and IgM isotypes. Most of the IgG anti-Sm antibodies were detected in SLE sera, but they were found also in two sera of MG and in one sera of RA patients. IgM anti-Sm antibodies were not found in SLE sera, but they were detected in low titer in MG, RA and autoimmune thyroid diseases. The activity against RNP and/or Sm was further confirmed by employing immunoblotting assays. In none of the patients, except those with SLE, was any clinical manifestation of SLE noted. The mere presence of anti-Sm antibodies of the IgG isotypes is not sufficient for the development of SLE, however, its presence is highly specific for SLE.

Adult↗
PubMed1990

Down-regulation of autoantibody levels of cyclosporine and bromocriptine treatment in patients with uveitis.

The administration of cyclosporine A, cyclosporine A plus bromocriptine, or bromocriptine results in down-regulation of antinuclear autoantibody levels in the sera of patients with uveitis. Decreased levels of autoantibodies against DNA, histones, cardiolipin, RNP, Sm, Ro (SS-A), and La (SS-B) were detected in the sera of patients with uveitis receiving cyclosporine A or cyclosporine A plus bromocriptine following 3 months of treatment. In contrast to the decreased antibody titers obtained following the treatment, the total immunoglobulin levels remained within the normal range. The results indicate that cyclosporine may affect B cell function, thereby yielding the observed decrease in autoantibody levels. This phenomenon might have clinical importance as a serological indicator of the efficiency of the patients to respond to the drug.

Autoantibodies↗
PubMed1990

Induction of experimental systemic lupus erythematosus in mice by immunization with a monoclonal anti-La autoantibody.

Experimental systemic lupus erythematosus (SLE) in mice can be induced by immunization either with a human monoclonal anti-DNA antibody bearing the 16/6 idiotype (16/6 Id) or with a mouse monoclonal anti-idiotypic antibody specific for the 16/6 Id. In the present report we investigated the pathogenic role of a monoclonal anti-La autoantibody in the induction and mediation of experimental SLE in mice. The monoclonal anti-La antibody was derived from a mouse in which experimental SLE was induced by immunization with the monoclonal anti-16/6 Id antibody. Following immunization with the anti-La antibody the mice produced antibodies to double-stranded DNA, single-stranded DNA, Sm, SS-A/Ro, SS-B/La, and ribonucleoprotein. Furthermore, even though the anti-La antibody does not express nor react with the 16/6 Id, the immunized mice produced high titers of anti-16/6 Id antibodies as well as 16/6 Id bearing antibodies. Four months following immunization the mice exhibited significant proteinuria, and kidney sections revealed immune complex deposits on the basement membrane of the glomeruli. These results suggest that anti-La autoantibodies are involved in the induction and mediation of SLE in mice.

Animals↗