Resistance/susceptibility to Echinococcus multilocularis infection and cytokine profile in humans. I. Comparison of patients with progressive and abortive lesions

Citation
V. Godot et al., Resistance/susceptibility to Echinococcus multilocularis infection and cytokine profile in humans. I. Comparison of patients with progressive and abortive lesions, CLIN EXP IM, 121(3), 2000, pp. 484-490
Citations number
28
Categorie Soggetti
Immunology
Journal title
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
ISSN journal
00099104 → ACNP
Volume
121
Issue
3
Year of publication
2000
Pages
484 - 490
Database
ISI
SICI code
0009-9104(200009)121:3<484:RTEMIA>2.0.ZU;2-U
Abstract
To clarify the role of Th1- and Th2-type cytokines in the various outcomes of human alveolar echinococcosis (AE), the cytokine immune response of self -cured patients was studied and compared with those of progressive AE patie nts and healthy subjects. Self-cured patients were divided into two groups according to the following clinical features: subjects who had positive Ech inococcus multilocularis serologies and hepatic calcifications typical of A E were classified as 'abortive AE' patients, and those who had positive E. multilocularis serologies but no hepatic lesions or calcifications detectab le by ultrasonography were classified as 'positive serology' subjects. Secr etions of IL-5, IL-10 and interferon-gamma, and expression of IL-5 mRNA wer e evaluated in peripheral blood mononuclear cells (PBMC) stimulated in vitr o with the mitogen phytohaemagglutinin-C or specific E. multilocularis anti genic preparations. The cytokine profile of abortive AE patients was the op posite of that observed in progressive AE patients. An intermediate profile was observed in positive serology subjects. PBMC from abortive AE patients , whether non-stimulated or stimulated with PHA and antigenic preparations, secreted significantly lower levels of IL-10 than those isolated from prog ressive AE patients. Our observations seem to confirm the regulatory role o f IL-10 in the immunopathology of human AE.