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Infection and Immunity, June 1999, p. 3014-3018, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Interleukin 5 (IL-5) Is Not Required for Expression of a Th2
Response or Host Resistance Mechanisms during Murine Schistosomiasis
Mansoni but Does Play a Role in Development of IL-4-Producing
Non-T, Non-B Cells
Laura
Rosa Brunet,1,
Elizabeth A.
Sabin,1,
Allen W.
Cheever,2
Manfred A.
Kopf,3 and
Edward J.
Pearce1,*
Department of Microbiology and Immunology,
College of Veterinary Medicine, Cornell University, Ithaca, New
York 148531; Biomedical Research
Institute, Rockville, Maryland 208522; and
Basel Institute for Immunology, Basel,
Switzerland3
Received 12 November 1998/Returned for modification 17 December
1998/Accepted 26 March 1999
During schistosomiasis, interleukin-5 (IL-5)-dependent eosinophil
responses have been implicated in immunopathology, resistance to
superinfection, synergistic interactions with chemotherapeutic agents,
and the inductive phase of the egg-induced Th2 response. We examined
these issues in IL-5-deficient (IL-5
/
) mice.
IL-5
/
and wild-type (WT) mice were indistinguishable in
terms of susceptibility to primary infections and the ability to resist
secondary infections. Moreover, hepatic pathology was similar in both
strains apart from a relative lack of eosinophils and, during chronic
infection, a significantly larger mast cell component in the granulomas
of IL-5
/
mice. Splenocyte cytokine production in
response to soluble egg antigen (SEA) or anti-CD3 revealed no
significant differences except for heightened tumor necrosis factor
alpha production by cells from chronically infected
IL-5
/
mice compared to WT animals. In contrast,
ionomycin-stimulated non-B, non-T (NBNT) cells from
IL-5
/
mice produced significantly smaller IL-4 amounts
than did NBNT cells from WT animals. This difference was not apparent
following plate-bound anti-immunoglobulin E or SEA stimulation. The
absence of IL-5 failed to affect the induction of Th2 responses in
naive mice. Peritoneal exudate cells recovered from egg-injected
IL-5
/
or WT mice produced equivalent levels of IL-4
following restimulation with SEA or anti-CD3.
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, C5-165 VMC, College of Veterinary
Medicine, Cornell University, Ithaca, NY 14853-6401. Phone: (607)
253-3389. Fax: (607) 253-3384. E-mail: ejp2{at}cornell.edu.

Present address: Department of Pathology, Cambridge University,
Cambridge, United Kingdom CB2
1QP.

Present address: JAVMA, Schaumburg, IL 60173-4360.
Infection and Immunity, June 1999, p. 3014-3018, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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