Biomedical subjects
L Prin
Publications and source records attributed to L Prin.
[Hypereosinophilia: from basic data to clinical aspects].
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[Hypereosinophilic syndrome in a HIV I+ patient].
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[Investigation of chronic hypereosinophilia: new perspectives].
In some circumstances and despite investigations, no aetiology is found for hypereosinophilia. This becomes of particular concern when hypereosinophilia is elevated and persistent. While some chronic hypereosinophilias signal the onset of malignant haemopathies, others remain unexplained for up to several years. But all may cause severe complications to the viscera, among which cardiopathies, and in particular endomyocardial fibrosis, are predominant. New data on chronic unexplained hypereosinophilia point to regulation defects in eosinophils or more often in T lymphocytes. Thanks to simple investigations such as flow cytometry, along with other more sophisticated procedures, we should soon be better equipped to classify chronic hypereosinophilia and, in the long term, to define more adequate strategies for treatment.
[Relevance of anti-tissue transglutaminase antibodies in coeliac disease diagnosis].
Coeliac disease is precipitated upon exposure to the dietary wheat gluten. Definitive diagnosis relies on intestinal biopsy and regression of clinical and histological disorders with adherence to a gluten-free diet. Coeliac disease is usually associated with a malabsorption syndrome. However, both atypical and silent clinical forms have been recently described and prevalence of the disease may be under-estimated. Serological tests have been developed in order to select candidates for intestinal biopsy, but these biological parameters are not suitable for screening in the general population. Indeed, antigliadin IgG antibodies have a poor specificity. antigliadin IgA antibodies a poor sensitivity. The detection of antiendomysial IgA antibodies (EmA) by immunofluorescence, although considered as the "gold standard" of serological coeliac disease markers, could not be automated, depends on a subjective fluorescence display, and may be limited by the degree of training of the observer. In year 1997, tissue transglutaminase (tTg) has been identified as the main autoantigen recognized by EmA. On this basis, solid-phase enzyme-linked immunosorbent assays (Elisa) have been developed in order to potentially replace the EmA assay. Several commercial kits are now available but their diagnostic performances have not yet been compared. We selected 75 sera, including sera from 26 patients with coeliac disease in order to evaluate five commercial anti-tTG Elisa kits. For all patients, treated or not, detection of anti-tTG antibodies with four of the five tested kits correlates with EmA test. Kits using human tTG have the highest specificity, equivalent to the value of EMA test, and widely better than antigliadin antibodies. Anti-tTG Elisa kits using human tTG may be used as an alternative way to the EmA assay in the next future, and may supplant IgA anti-gliadin antibodies for coeliac disease screening.
Induction of CD23, CD25 and CD4 expression on an eosinophilic cell line (EoL-3) by interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-5 (IL-5).
The effects of IL-3, GM-CSF and IL-5 on the expression of CD23 (Fc epsilon RII), CD25 (IL-2R/p55) and CD4 on an eosinophilic cell line (EoL-3) were investigated by flow cytometry. A separate incubation with IL-3, GM-CSF or IL-5 alone, did not induce the expression of CD23, CD25, or CD4. However, a sequential incubation with IL-3 for 6 days, then with IL-3 and GM-CSF for the following 6 days, induced a significant expression of CD23 and CD25. After a further incubation for 6 days with IL-3, GM-CSF and IL-5, CD4 was then expressed, while CD23 and CD25 expression still increased. The kinetics of expression of CR3/CD11b were parallel to that of CD23, but the expression of the transferrin receptor (CD71) remained negative. Northern blot analysis revealed the presence of mRNA encoding CD23, CD25 and CD4 in EoL-3 stimulated by IL-3, GM-CSF and IL-5. Culture with GM-CSF induced the binding of radiolabeled IL-5 to EoL-3 cells, with an increased affinity after incubation with IL-3, GM-CSF and IL-5. These data indicate that IL-3, GM-CSF and IL-5, might be involved in the expression of functional markers on eosinophil membrane.