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A popular hypothesis to explain parasite survival in the presence of a pronounced T helper 2 phenotype in helminth-parasitized populations has been Fc
RI blockade by parasite-induced polyclonal IgE. To begin to test the hypothesis that Fc
RI-bearing cells would be refractory to activation in parasitized populations, we investigated basophil function in 43 individuals from a hookworm endemic area. Study individuals had high levels of total IgE and eosinophilia and a mean hookworm burden of 2,257 epg. Basophils from all members of this parasitized population were shown to release histamine to a number of agonists, including anti IgE and a hookworm allergen, calreticulin. These data would indicate that Fc
RI blockade at the level of the basophil did not occur in this parasitized population despite the presence of possible immunologic blocking agents. This would suggest that this effector arm of the T helper 2 phenotype remains operative in infected populations.
Received December 6, 2006. Accepted for publication July 3, 2007.
Acknowledgments: Fieldwork was supported by the Wellcome Trust and RJQ was supported by a MRC Career Development Award. We thank Moses Lagog (Papua New Guinea Institute of Medical Research) for technical support in the field, and the inhabitants of Haven and Wasab for their kind participation.
* Address correspondence to Alan Brown, University Park, Notting-ham, NG7 2RD. E-mail: alan.brown{at}nottingham.ac.uk
Authors addresses: David I. Pritchard, Doreen S. W. Hooi, Alan Brown, and Rebecca Caddick, The Boots Institute, School of Pharmacy, University of Nottingham, NG7 2RD. Telephone: +44 115 9516165. Fax: + 44 115 9515122. Moses J. Bockarie, Papua New Guinea Institute of Medical Research, Madang Province, Papua New Guinea. Rupert J. Quinnell, Institute of Integrative and Comparative Biology, University of Leeds, Leeds, LS2 9JT.
Reprint requests: Alan Brown, University Park, Nottingham, NG7 2RD. E-mail: alan.brown{at}nottingham.ac.uk
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