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Infection and Immunity, December 2001, p. 7743-7752, Vol. 69, No. 12
Department of Pathology, University of
Connecticut Health Center, Farmington,
Connecticut,1 and Jackson
Laboratories, Bar Harbor, Maine2
Received 2 May 2001/Returned for modification 2 July 2001/Accepted 4 September 2001
Interleukin-4 (IL-4) has been shown to be crucial in parasite
expulsion in several gastrointestinal nematode infection models. Data
from both epidemiological studies with humans and experimental infections in animals imply a critical role for the type II helper response, dominated by IL-4, in host protection. Here we utilized inbred mice on two distinct backgrounds to document the involvement of
IL-4 in the clearance of a primary infection of Brugia
from the murine host. Our data from infections of IL-4
receptor
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.12.7743-7752.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Interleukin-4 Receptor-Stat6 Signaling in Murine
Infections with a Tissue-Dwelling Nematode Parasite
/
and Stat6
/
mice further
indicate that IL-4 exerts its effects by activating the Stat6 molecule
in host target cells, a finding which links clearance requirements of a
gastrointestinal tract-dwelling nematode with those of a
tissue-dwelling nematode. Additionally, we show that the requirements
for IL-4 receptor binding and Stat6 activation extend to accelerated
clearance of a secondary infection as well. The data shown here,
including analysis of cell populations at the site of infection and
infection of immunoglobulin E (IgE)
/
mice, lead us to
suggest that deficiencies in eosinophil recruitment and isotype
switching to IgE production may be at least partially responsible for
slower parasite clearance in the absence of IL-4.
*
Corresponding author. Mailing address: Department of
Pathology, University of Connecticut Health Center, 263 Farmington
Ave., Farmington, CT 06030-3105. Phone: (860) 679-3221. Fax: (860)
679-2936. E-mail: rajan{at}neuron.uchc.edu.
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