Schistosoma mansoni in IL-4-deficient mice

118Citations
Citations of this article
34Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Immunopathology and immune responses to Schistosoma mansoni were examined in IL-4 -/- mice. IL-5 and IL-10 production by lymphoid cells stimulated with soluble egg antigen (SEA), peripheral eosinophilia and serum levels of soluble IL-4 receptor but not IgE were all significantly elevated over background normal levels in IL-4 -/- mice as a result of infection. Additionally, IL-10 and IL-5 in addition to IL-2 and IFN-γ transcripts were equally evident in diseased liver tissue from infected IL-4 -/- and wild-type mice. Nevertheless, analysis of antigen-stimulated IL-2, IL-4, IL-5, IL-10 and IFN-γ production by lymphoid organ cells from infected or egg-injected IL-4 -/- mice revealed a more T(h)1-like pattern of cytokine production (IFN-γ > IL-5) than in (wild-type) mice in which a stronger type 2 response to SEA was detectable (IL-4, IL-5 > IFN-γ). Despite this, at 8 and 16 weeks after infection, liver pathology, as indicated by the size, cellularity, cellular composition and collagen content of granulomas, was similar in IL-4 -/- and wild-type animals. As in wild-type animals, granuloma size at week 16 was smaller than at week 8, indicating that modulation had occurred in the absence of IL-4. Differences in pathology were seen only when eggs were experimentally embolized to the lungs, in which case IL-4 -/- mice made smaller granulomatous responses than did wild-type animals. These data clearly show that IL-4 is not necessary for the hepatic granuloma formation which occurs during experimental schistosomiasis.

Author supplied keywords

Cite

CITATION STYLE

APA

Pearce, E. J., Cheever, A., Leonard, S., Covalesky, M., Fernandez-Botran, R., Kohler, G., & Kopf, M. (1996). Schistosoma mansoni in IL-4-deficient mice. International Immunology, 8(4), 435–444. https://doi.org/10.1093/intimm/8.4.435

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free