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Regulation of anti-filarial IgE by infection pressure

Published online by Cambridge University Press:  05 August 2002

A. J. TERHELL
Affiliation:
Department of Parasitology, Leiden University Medical Centre, P.O. Box 9605, 2300 RC, Leiden, The Netherlands
W. A. STOLK
Affiliation:
Department of Public Health, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR, Rotterdam, The Netherlands
M. HAARBRINK
Affiliation:
Department of Parasitology, Leiden University Medical Centre, P.O. Box 9605, 2300 RC, Leiden, The Netherlands
A. MANGALI
Affiliation:
Department of Parasitology, Hasanuddin University, Kampus Tamalanrea, Jl. Perintis Kemerdekaan, Makassar, Sulawesi, Indonesia
G. J. VAN OORTMARSSEN
Affiliation:
Department of Public Health, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR, Rotterdam, The Netherlands
M. YAZDANBAKHSH
Affiliation:
Department of Parasitology, Leiden University Medical Centre, P.O. Box 9605, 2300 RC, Leiden, The Netherlands

Abstract

In lymphatic filariasis, specific IgG4 responses to the parasite and their relationship with infection have been studied extensively, but only a few studies have concentrated on anti-filarial and total IgE. Here we have investigated the role of filarial infection pressure on production of IgE by considering length of exposure (age), filarial endemicity and parasitological status. Antibody levels were determined in 366 individuals, who were resident in 3 villages in South-Sulawesi, Indonesia, with varying degrees of filarial transmission intensity, as indicated by the prevalence of Brugia malayi microfilaraemia (0·7%, 9% and 32%, respectively). Anti-filarial IgE levels were significantly lower in the low transmission village than in the areas with intermediate and high filarial transmission; however, in the latter village a remarkable suppression of specific IgE was found. Microfilaria-positive individuals showed elevated levels of total IgE, but suppression of specific IgE, which has been reported before. Taken together, these observations suggest that 2 opposing mechanisms regulate anti-parasite IgE expression: increasing experience of filarial infection stimulates specific IgE, but antibody levels become specifically suppressed when microfilariae or adult worms develop. Using a simple mathematical model, we illustrate how anti-filarial IgE increases with parasite antigen up to a threshold level, but levels off and becomes down-regulated after the threshold is exceeded.

Type
Research Article
Copyright
2002 Cambridge University Press

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