Biomedical subjects

J C Torre-Alonso

Publications and source records attributed to J C Torre-Alonso.

3 recordsLinked to original sources

PubMed1996

Annexin V autoantibodies in rheumatoid arthritis.

OBJECTIVE: To investigate the occurrence of anti-annexin V autoantibodies in sera of patients with rheumatoid arthritis to assess involvement with the disease and any relation to glucocorticoid treatment. METHODS: Anti-annexin V antibodies were measured by an enzyme linked immunosorbent assay (ELISA) which used the purified human recombinant protein as antigen. RESULTS: Concentrations of anti-annexin V autoantibodies, predominantly of the IgG class, were significantly raised in sera from patients with rheumatoid arthritis compared to normal controls. This was not correlated with other indices of disease activity such as erythrocyte sedimentation rate or C reactive protein and was unrelated to glucocorticoid treatment. CONCLUSIONS: Extracellular annexin V provides an antigenic stimulus for autoantibody production and its in vivo expression is independent of glucocorticoid control. Such autoantibodies may have a detrimental role in the arthritic condition by interfering with putative functions of annexin V, including collagen type II binding, inhibition of phospholipase A2 activity, and Fc receptor activity.

Adult↗

PubMed1995

Upregulated expression of IL-4 receptors and increased levels of IL-4 in rheumatoid arthritis patients.

The level of IL-4R expression on peripheral lymphocyte subsets from rheumatoid arthritis (RA) patients and controls was studied by flow cytometric analysis of the binding of phycoerythrin-labelled IL-4 (PE-IL-4). In normal lymphocytes, IL-4R is mainly expressed on CD19+ cells, although it was also seen, at lower levels, on CD3+, CD4+ and CD8+ cells. In RA patients, a significantly increased spontaneous expression of IL-4R was observed, compared with controls, in the CD3+, CD4+ and CD19+ cell subsets. No significant differences in IL-4R expression were found between patients receiving steroids and those who were not, suggesting that steroids are not involved in upregulating IL-4R levels in vivo. Because IL-4 is a potent upregulator of IL-4R, we considered the possibility that incremented levels of circulating IL-4 in RA accounted for the high surface expression of IL-4R. By ELISA, we found abnormally high levels of immunoreactive IL-4 in 35.13% of patient serum samples, while it was undetectable in control sera. In addition, we examined IL-4 mRNA expression by polymerase chain reaction (PCR) in the PBMC of patients and controls. IL-4 PCR products were observed in four out of 10 patients studied but in none of the controls. No correlation was observed between the seric concentrations of IL-4 and IL-4R, indicating that activator factors other than IL-4 contribute to the upregulation of IL-4R expression in RA. Since the patients' sedimentation rate and CRP values did not correlate with the concentration of circulating IL-4, we conclude that this lymphokine does not contribute to the deleterious effect of the disease. Rather, due to its antiinflammatory properties, the overproduction of IL-4 in RA may be a compensatory mechanism neutralizing the harmful effect of activated macrophages.

Aged↗

PubMed1994

Decrease in detectable complement receptor type 1 levels on erythrocytes from patients with psoriatic polyarthritis.

The complement receptor type 1 (CR1) levels on erythrocyte membranes from 23 patients with PsA was determined by using ELISA. Six patients had an axial form, the rest had peripheral arthritis (10 polyarthritis and seven oligoarthritis). A significant decrease in levels of this receptor was found in patients with polyarthritis compared with healthy controls. Non-significant differences were found when comparing the other two groups of patients with the controls, although the mean values of CR1 were lower in the patients' group. We also found an inverse correlation between CR1 levels and articular index, but not with ESR, CRP or disease duration. No differences in the CR1 density were obtained for HLA-B27 positive and HLA-B27 negative patients.

Adult↗