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Biomedical subjects

Y Shoenfeld

Publications and source records attributed to Y Shoenfeld.

At least 577 records · Page 32Linked to original sources
PubMed1992

A multidimensional autoantibody analysis specifying systemic lupus erythematosus patients with neuropsychiatric symptomatology.

Utilizing a newly perfected multiple-response permutation procedure, we analyzed the autoantibody titer of systemic lupus erythematosus (SLE) patients during active and convalescent periods of disease, SLE patients without neurological involvement, and three other comparison groups (patients with active tuberculosis, patients with multiple sclerosis, and healthy normal controls). The multidimensional analysis we used distinguished those SLE patients with neurological involvement from the other SLE patients. Differences were noted by a univariate analysis measuring antibodies to single- and double-stranded DNA, poly (G), Sm, RNP, Ro, La, and gangliosides. Elevated concentrations of the common anti-DNA idiotype 16/6 were also noted among SLE patients with neuropsychiatric illness. This report stresses that increased disease activity in SLE patients with neuropsychiatric phenomena is reflected by their autoantibody profile.

Antibodies, Antinuclear↗
PubMed1992

The detection of anti-Ro/SS-A and anti-La/SS-B activity of human serum monoclonal immunoglobulins (monoclonal gammopathies).

The sera of 340 patients with monoclonal gammopathies were examined for the presence of anti-Ro/SS-A and anti-La/SS-B activity. An enzyme-linked immunosorbent assay (ELISA) technique was employed. Forty-six sera (13.5%) bound to Ro/SS-A, while 79 sera (23.2%) bound to La/SS-B. The anti-Ro/SS-A and anti-La/SS-B antibodies were found in sera of patients with IgG, IgM, and IgA gammopathies. Forty-two of the 46 sera (91.3%) with positive anti-Ro/SS-A activity were found to bind La/SS-B as well, while only 53.2% (42 out of 79) of the sera that had anti-La/SS-B activity also bound Ro/SS-A. The activity against Ro/SS-A and La/SS-B was further confirmed by immunoblotting with purified immunoglobulins. Antibodies to Ro/SS-A and La/SS-B are common in systemic lupus erythematosus, Sjögren's syndrome, and other rheumatic disorders. Yet none of the patients whose serum was found to contain high titres of anti-Ro/SS-A or anti-La/SS-B human monoclonal antibodies presented with symptoms related to such autoimmune diseases. Our results of a high incidence of anti-Ro/SS-A or anti-La/SS-B activity in the sera of patients with monoclonal gammopathies support previous reports of autoantibody properties characteristic of these immunoglobulins.

Antibodies, Antinuclear↗
PubMed1991

Modulation of SLE induction in naive mice by specific T cells with suppressor activity to pathogenic anti-DNA idiotype.

T cells (CD8+) with specific suppressor activity against anti-dsDNA antibody (16/6 Id+) were generated in vitro. The cells were established from BALB/c-enriched T cells exposed in vitro to silica beads coated with the pathogenic anti-DNA idiotype, 16/6. The idiotype specificity of the suppressor cells was demonstrated by (a) specific induction of a decrease in proliferative response of T helper cell lines specific for the pathogenic idiotype (16/6 Id), when exposed to the idiotype, with no effect on T cell lines with other specificities, e.g., against human IgM or synthetic polypeptide. (b) Effectively suppressing in vitro antibody production of anti-16/6 antibody, employing 16/6-primed B cells and specific helper T cell line. The 16/6 Id-specific Ts cells were found to be MHC restricted. Weekly intravenous injections of 10(7) 16/6 Id-specific Ts cells given to BALB/c mice at different stages of experimental SLE disease prevented the clinical, serological, and pathological manifestations. This effect was characterized by decreased titers of autoantibodies (e.g., anti-DNA, anti-Sm antibodies) in the sera, by abolishment of the proteinuria, leukopenia, and the increased ESR, followed by decreased immunoglobulin deposition in the kidneys. Treating the mice with control IgM-specific T cells did not affect the above parameters. These studies demonstrate the ability to generate Ts cells specific for pathogenic idiotypes. The method might be employed therapeutically to modulate the course of autoimmune conditions.

Animals↗
PubMed1991

The effects of incubation temperature and coating procedure on the measurement of antibodies to cardiolipin.

Many laboratories have established ELISAs for the the routine detection of anti-cardiolipin antibodies (ACA). Earlier studies had indicated that assay incubation at 37 degrees C may interfere with the antigen binding capacity of these antibodies. We have reexamined this phenomenon by comparing ACA titers obtained when incubations are performed at either 37 degrees C or at room temperature (RT). In addition, the effect of coating antigen in aqueous or organic solution was compared. The sera tested included a set of recognized ACA standards and samples from 19 patients with SLE, two with primary anti-phospholipid syndrome, 71 patients with a variety of autoimmune and non-autoimmune disorders and 210 blood bank controls. The results show that while some sera do perform better under either incubation temperature there was no correlation between ACA titers and incubation temperature on a population basis either for IgG or IgM isotypes. This was seen both for positive standards and patient sera. For IgG ACA a similar phenomenon was seen if the microplates were coated with cardiolipin either in sodium carbonate or ethanol. For IgM ACA there was a significant increase in ACA titers at RT when cardiolipin was coated in ethanol. The data suggest that for most sera neither the antigen coating medium nor the assay incubation temperature are important variables in the determination of IgG ACA. Factors contributing to the influence of either variable in individual sera could not be identified.

Analysis of Variance↗
PubMed1991

Induction of anti-phospholipid syndrome in naive mice with mouse lupus monoclonal and human polyclonal anti-cardiolipin antibodies.

The primary anti-phospholipid syndrome is characterized by recurrent venous and arterial thromboembolic phenomena, recurrent fetal loss, thrombocytopenia, and serological evidence of anti-cardiolipin (aCL) antibodies or/and the presence of lupus anticoagulant (prolonged activated partial thromboplastin time). The exact role of aCL antibodies in pathogenesis is not clear and the mechanism by which the antibodies may induce the various manifestations is unknown. In the current study we evaluated the effect of passive transfer of aCL antibodies (to the tail vein of naive mice) on fecundity, fetal loss (fetal resorption), and the weight of embryos and placentae. Two types of aCL antibodies were employed: (i) mouse monoclonal aCL antibodies derived from a BALB/c mouse in which experimental systemic lupus erythematosus was induced by a pathogenic idiotype (idiotype 16/6) of anti-DNA antibodies and (ii) polyclonal IgG and IgM aCL antibodies derived from serum of a patient with primary anti-phospholipid syndrome. After infusion of either antibody (10 micrograms per mouse) we could demonstrate lower fecundity rate, increased resorption index of embryos (equivalent to recurrent fetal loss), lower number of embryos per pregnancy, and lower mean weights of embryos and placentae in comparison to mice infused with appropriate control immunoglobulins. We conclude that the aCL antibodies may have direct effects on fecundity and on the outcome of pregnancy.

Animals↗